The DOI matches its Crossref record; 152 of the 152 references it cites were found in a registry or an index; 127 of the 201 sources its claims cite were checked for support.
Aging, Cellular Senescence, and Cancer
Open accessAbstract
For most species, aging promotes a host of degenerative pathologies that are characterized by debilitating losses of tissue or cellular function. However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer. In contrast to the loss of function that characterizes degenerating cells and tissues, malignant (cancerous) cells must acquire new (albeit aberrant) functions that allow them to develop into a lethal tumor. This review discusses the idea that, despite seemingly opposite characteristics, the degenerative and hyperplastic pathologies of aging are at least partly linked by a common biological phenomenon: a cellular stress response known as cellular senescence. The senescence response is widely recognized as a potent tumor suppressive mechanism. However, recent evidence strengthens the idea that it also drives both degenerative and hyperplastic pathologies, most likely by promoting chronic inflammation. Thus, the senescence response may be the result of antagonistically pleiotropic gene action.
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Claims the paper makes
37 Partly supported · 33 Own interpretation · 25 No basis given · 24 Supported · 19 No full text of the sources · 8 Supported so far · 5 Not checked yet · 4 Mixed support · 1 Sources not found · accuracy not yet measured
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“the effects of the senescent fibroblasts were due primarily to their secretion of matrix metalloproteinases (MMPs), which are prominent SASP components (32, 94).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE, AGING, AND CANCER: THE DARK SIDE > Senescent Cells and Degenerative Phenotypes
What the sources say
- Disputedcites [32] sourceExperimental — accuracy not yet measured
In “SASPs Induce Epithelial–Mesenchyme Transitions and Invasiveness” (page unavailable), the paper reports that senescent fibroblast secretions promoted invasion, but identifies IL-6 and IL-8—not MMPs—as the SASP factors contributing substantially to that effect. Our copy does not identify MMPs as prominent SASP components or as the primary cause of these effects. (LLM, conf=0.82)
Checked by a reasoning model — may be wrong.
- Partly supportedcites [94] sourceExperimental — accuracy not yet measured
The Results section, “Members of MMP and Other Gene Clusters Comprise the Conserved SASP” (page not provided), identifies secreted MMPs as SASP components. The paper does not show that MMPs were primarily responsible for the disruptive effects in the cited cultures; its Discussion instead attributes much of the growth-stimulatory activity to CXCL-1. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Disputed
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“Finally, the SASP also includes proteins that can help senescent cells evade immune recognition and clearance (92, 93).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: THE BRIGHT SIDE > Immune Clearance
What the sources say
- Partly supportedcites [92] sourceExperimental — accuracy not yet measured
In “The Senescence-Associated Secretory Phenotype Affects Leukocyte Infiltration and Tumor Immunology” (page unavailable), the paper says molecules overexpressed by senescent fibroblasts can lead to an inadequate immune response near those cells. It does not say that these proteins help senescent cells themselves evade immune recognition or clearance; the discussion concerns immune responses in the tumor environment. (LLM, conf=0.85)
- Disputedcites [93] sourceExperimental — accuracy not yet measured
The “Multiple roles of the SASP” section says the SASP might signal the immune system to clear senescent cells. It also describes SASP-associated cytokines and enzymes promoting clearance in mouse models. The cited paper thus makes the contrary point, rather than identifying proteins that help senescent cells evade recognition or clearance. Page numbers were not available in our copy. (LLM, conf=0.84)
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“This finding may be complicated by the fact that the proliferative arrest of mouse cells cultured in ambient oxygen concentrations (approximately 20%), which is substantially higher than the oxygen concentrations to which cells are exposed in vivo, has only some features of the senescence response that is induced under more physiological oxygen concentrations (38, 94).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: THE BRIGHT SIDE > Tumor Suppression
What the sources say
- Disputedcites [38] sourceExperimental — accuracy not yet measured
The paper reports that mouse embryonic fibroblasts arrested and showed a senescent morphology in 20% oxygen. But in its discussion of growth at physiological 3% oxygen (Fig. 2a; page unavailable), it says the cells grew with little evidence of replicative senescence, rather than undergoing the contrasting senescence response described in the claim. It notes an exception for DNA-repair-deficient Balb/c cells, whose eventual senescence at 3% oxygen had a phenotype similar to that of cells grown at 20%. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
- Supportedcites [94] source
The Discussion (page not provided) says mouse cells arrested in 20% oxygen show some senescence features, including growth arrest and SA-βGal activity, but differ from mouse cells made senescent in physiological oxygen. The Results (page not provided) identify 20% oxygen as atmospheric culture conditions and 3% as physiological oxygen. (LLM, conf=0.94)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Disputed
Every source the paper cites for this claim was checked and supports it.
In the paper
“The permanence of the senescence growth arrest enforces the idea that the senescence response evolved at least in part to suppress the development of cancer (9).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: OVERVIEW
What the sources say
- Supportedcites [9] source
The Introduction describes senescence as an irreversible loss of proliferative capacity and places it among cellular mechanisms of tumor suppression that evolved to protect against cancer. The “Blocking Tumor Growth by Senescence” section reports experiments examining that protective role. Page numbers are not available in our copy. (LLM, conf=0.90)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, molecular biological manipulations, for example, the sequential inactivation of certain tumor suppressor genes, can cause senescent cells to proliferate (10).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: OVERVIEW
What the sources say
- Supportedcites [10] source
The Results report that WI-38 cells with p16 suppressed before senescence resumed proliferation after subsequent p53 inactivation; more than 70% proliferated. This supports the cited example of sequential molecular manipulations, though the result depends on when p16 is suppressed. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Many types of cytotoxic chemotherapies are severe DNA-damaging agents that can induce senescence in both tumor cells and surrounding normal cells (31–34).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES > Genomic Damage
What the sources say
- Partly supportedcites [31] sourceExperimental — accuracy not yet measured
The Results and Discussion (page not available) show that doxorubicin, a DNA-damaging anticancer drug, induced senescence in surviving colon carcinoma cells. The introduction (page not available) also says DNA damage can trigger senescence in normal cells and that various anticancer agents can induce senescence-like arrest in tumor cells. It does not establish that cytotoxic chemotherapies induce senescence in surrounding normal cells. (LLM, conf=0.86)
- Partly supportedcites [32] sourceExperimental — accuracy not yet measured
In “Chemotherapy-Induced SASPs Occur In Vivo,” the paper reports that the DNA-damaging chemotherapy mitoxantrone induced senescence in epithelial cell lines and normal fibroblasts in culture, and examines treated tumor cells in vivo. It does not establish that many types of chemotherapy induce senescence in normal cells surrounding tumors. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [33] source
- Partly supportedcites [34] sourceExperimental — accuracy not yet measured
The Introduction (page not supplied) says most conventional agents damage cellular components, often DNA, and that drug-induced damage can initiate senescence. The Discussion reports chemotherapy-induced senescence in a murine lymphoma model. Our copy does not establish that these agents cause severe DNA damage or induce senescence in surrounding normal cells. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Nevertheless, there is substantial overlap among SASPs; proinflammatory cytokines are the most highly conserved feature, cutting across many different cell types and senescence-inducing stimuli (33, 42, 96, 99, 100, 112–114).”
§ Aging, Cellular Senescence, and Cancer > SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE
What the sources say
- Not checked — no full text of the sourcecites [33] source
- Partly supportedcites [42] sourceExperimental — accuracy not yet measured
The passages labeled Abstract report IL-6 and IL-8 secretion in several fibroblast models and under multiple DNA-damaging conditions. They do not compare SASPs to establish that proinflammatory cytokines are their most highly conserved feature; the paper also reports that p16-induced senescence without DNA damage did not initiate a cytokine response. Page numbers are unavailable in our copy. (LLM, conf=0.87)
- Not checked — no full text of the sourcecites [96] source
- Partly supportedcites [99] sourceExperimental — accuracy not yet measured
The Results report proinflammatory cytokines among factors secreted during oncogene-induced senescence, and the Discussion describes CXCR2-binding chemokines as upregulated during both replicative and oncogene-induced senescence. The paper does not establish substantial overlap among SASPs across many cell types or show that proinflammatory cytokines are their most highly conserved feature. (LLM, conf=0.84)
- Partly supportedcites [100] sourceExperimental — accuracy not yet measured
The Results report that IL-6, IL-1α, IL-1β, and IL-8 were upregulated during oncogene-induced senescence in human fibroblasts and melanocytes. The Discussion also identifies cytokines and chemokines as prominent in that setting. The paper does not establish substantial overlap among SASPs across many senescence-inducing stimuli or show that proinflammatory cytokines are their most highly conserved feature. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [112] source
- Not checked — no full text of the sourcecites [113] source
- Not checked — no full text of the sourcecites [114] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The SASP is primarily a property of cells that senesce owing to, or accompanied by, genomic damage or epigenomic perturbation.”
§ Aging, Cellular Senescence, and Cancer > SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE > The SASP: Causes
What the sources say
- Partly supportedcites [115] sourceExperimental — accuracy not yet measured
The discussion (p. 7) says chronic DNA-damage signaling is required for a SASP and concludes that the SASP is a consequence of severe DNA damage rather than growth arrest alone. This supports the genomic-damage part of the claim, but the passages do not address epigenomic perturbation as a cause of the SASP. (LLM, conf=0.85)
- Partly supportedcites [32] sourceExperimental — accuracy not yet measured
The Results (Figure 1D) show that DNA damage sufficient to cause senescence induced a SASP, while a lower radiation dose did not. The Discussion likewise describes the SASP as a response to severe or irreparable damage. These passages support the genomic-damage part of the claim, but our copy does not establish epigenomic perturbation as another basis for the SASP. (LLM, conf=0.87)
- Not checked — no full text of the sourcecites [33] source
- Partly supportedcites [42] sourceExperimental — accuracy not yet measured
In the supplied copy’s Abstract (page not specified), persistent DNA damage correlates with secretion of inflammatory SASP factors, while p16-induced senescence without DNA damage does not initiate that cytokine response. The paper says DNA-damage signalling drives only a subset of SASP factors; it does not establish the claim for the SASP as a whole or address epigenomic perturbation. (LLM, conf=0.86)
- Partly supportedcites [67] sourceExperimental — accuracy not yet measured
The Introduction and Results link SASP activation to DNA-damage signaling and show that HDAC inhibition can induce SASP factors without detectable DNA breaks. But the Introduction and Discussion also state that cells unable to senesce can express SASP factors, so the paper does not establish that the SASP is primarily a property of cells that senesce under those conditions. Page numbers are unavailable in our copy. (LLM, conf=0.85)
- Partly supportedcites [94] sourceExperimental — accuracy not yet measured
The Results section, “Effect of O2 on DNA Damage and Genomic Instability” (page not available), reports that the SASP correlates with persistent DNA-damage foci in mouse cells, as in human cells. The paper does not establish epigenomic perturbation as a basis for the SASP, and its findings in the cells studied do not establish the claim’s broader “primarily a property” characterization. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [96] source
- Partly supportedcites [99] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports increased secretion of CXCR2-binding chemokines during replicative and especially oncogene-induced senescence, and says the DNA-damage response is central to both. It does not establish that the SASP is primarily limited to cells with genomic damage, or link it to epigenomic perturbation. (LLM, conf=0.82)
- Partly supportedcites [100] sourceExperimental — accuracy not yet measured
The paper’s Summary links oncogene-induced senescence to an inflammatory transcriptome and secretion of IL-6. The Introduction discusses DNA-damage signaling in oncogene-induced senescence, and the passage headed “IL-6 Depletion Correlates with Reduced Formation of SAHF” reports chromatin changes. These passages do not establish that the SASP is primarily a property of cells senescing with genomic damage or epigenomic perturbation across senescence types. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [112] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Chronic inflammation, of course, is a cause of—or an important contributor to—virtually every major age-related disease, both degenerative and hyperplastic (109–111).”
§ Aging, Cellular Senescence, and Cancer > SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE
What the sources say
- Partly supportedcites [109] sourceExperimental — accuracy not yet measured
The Introduction calls chronic inflammation a major underlying condition of many age-related diseases, including degenerative conditions and cancer. The Conclusion likewise describes it as a primary factor underlying numerous age-related diseases. Neither passage supports the stronger claim that it contributes to virtually every major age-related disease. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [110] source
- Partly supportedcites [111] sourceExperimental — accuracy not yet measured
The Introduction and Conclusions and Prospective sections (page unavailable) describe chronic inflammation as a contributor to cancer risk and tumor development. They do not support the broader claim about virtually every major age-related disease, including degenerative diseases. (LLM, conf=0.87)
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“many SASP components directly or indirectly promote inflammation (59, 92, 93, 107, 108).”
§ Aging, Cellular Senescence, and Cancer > SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE
What the sources say
- Not checked — no full text of the sourcecites [59] source
- Supportedcites [92] sourceExperimental — accuracy not yet measured
In the section on soluble signaling factors, the paper identifies several SASP components as inflammatory cytokines, including IL-6 and IL-1. The sections on leukocyte infiltration and cell differentiation describe SASP factors acting on neighboring cells and recruiting inflammatory and immune cells, supporting both direct and indirect effects. Page numbers were not available in our copy. (LLM, conf=0.91)
- Supportedcites [93] source
The section “Senescent cells as a source of chronic inflammation” identifies numerous SASP proteins known to stimulate inflammation. “Chronic inflammation might propel basic aging processes” also describes an indirect route: senescent-cell cytokines attract and activate innate immune cells. (LLM, conf=0.93)
- Supportedcites [107] sourceExperimental — accuracy not yet measured
The ‘Secretory phenotype of senescent cells’ section describes the SASP as having pro-inflammatory effects and identifies inflammatory cytokines among its components. The ‘Regulation of the inflammatory component of the SASP’ section describes an indirect route: IL-1α promotes expression of IL-6 and IL-8. (LLM, conf=0.91)
- Supportedcites [108] sourceExperimental — accuracy not yet measured
The “Cellular senescence” section describes the senescent secretory phenotype as including inflammatory cytokines, ECM-modifying proteases, and reactive oxygen species. It also explains that substances released by senescent cells attract and activate immune cells, supporting both direct and indirect contributions to inflammation. (LLM, conf=0.91)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 26
- Probably not a substantial claim. 9
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“Dysfunctional telomeres elicit a DNA damage response (DDR) but suppress attempted DNA repair (22–25).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES > Telomere Shortening
What the sources say
- Not checked — no full text of the sourcecites [22] source
- Not checked — no full text of the sourcecites [23] source
- Supportedcites [24] source
The Results section ('Persistent DDR foci are localized at telomeres') says telomeric proteins inhibit DNA repair at chromosome ends. The Discussion says damaged telomeric tracts resist repair, while the Results section on ageing describes unrepaired telomeric breaks producing persistent DDR foci. Page numbers are not available in the supplied copy. (LLM, conf=0.93)
- Disputedcites [25] sourceExperimental — accuracy not yet measured
The paper reports that dysfunctional taz1Δ telomeres undergo a DNA damage response, supporting the first half of the claim. But it says DNA repair proteins accumulate at those chromosome ends and concludes, “Thus, DNA repair is ongoing at taz1Δ chromosome ends” (Abstract; page not supplied). It describes suppression of checkpoint signaling and cell-cycle arrest, not suppression of repair at these dysfunctional telomeres. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Dysfunctional telomeres appear to be irreparable; consequently, cells with such telomeres experience persistent DDR signaling and p53 activation (24, 26), which enforce the senescence growth arrest (Figure 2).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES > Telomere Shortening
What the sources say
- Supportedcites [24] source
The Discussion proposes that irreparable telomeric damage causes persistent DDR signaling and cellular senescence. In the Results (page unavailable), linear telomeric DNA sustained p53 Ser15 phosphorylation and growth arrest in human fibroblasts; separate irradiation experiments found that sustained DDR signaling was necessary to maintain senescence. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites [26] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Hence, the idea that the senescence response is tumor suppressive, although still speculative 50 years ago, was more firmly grounded (9).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES
What the sources say
- Supportedcites [9] source
In “Blocking Tumor Growth by Senescence” (page not supplied), Sager describes experiments examining senescence’s role in tumor suppression and concludes that senescence blocks tumor formation. This supports the cited point that the idea had gained an experimental grounding; the 50-year comparison is the citing authors’ historical framing. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In the case of telomeres, repair followed by cell division will cause rampant genomic instability through cycles of chromosome fusion and breakage (20, 21)—major risk factors for developing cancer.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES > Telomere Shortening
What the sources say
- Not checked — no full text of the sourcecites [20] source
- Partly supportedcites [21] sourceExperimental — accuracy not yet measured
Section 2 (p. 7) describes DNA repair systems fusing dysfunctional or uncapped telomeres, followed by mitotic breakage and cycles of fusion that cause genomic instability. Section 7 (pp. 15–16) links this instability to cancer, but specifies that it arises when cells with dysfunctional telomeres divide despite tumor-suppressor checkpoints. The claim omits the dysfunctional-telomere condition and makes repair at telomeres sound generally harmful. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Although drug-treated BubR1H/H;INK-ATTAC mice did not live longer, they were remarkably protected from several other age-related pathologies, including cataracts, sarcopenia, and loss of subcutaneous fat (128).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE, AGING, AND CANCER: THE DARK SIDE > Senescent Cells and Degenerative Phenotypes
What the sources say
- Supportedcites [128] source
The main text reports that AP20187 treatment from weaning delayed cataracts and lordokyphosis, preserved muscle function, and prevented fat loss, including subdermal fat loss (Fig. 2b–h). It also says overall survival was not substantially extended (Supplementary Fig. 5d). The cataract finding applies to treatment begun early in life; cataracts were unchanged when treatment began at five months. (LLM, conf=0.93)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- The authors state this as an assumption: Cells that express p16INK4a are senescent.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“That is, the rapid robust DDR that occurs immediately after DNA damage does not induce a SASP; rather, the SASP develops slowly—over several days in culture—and only after the initial DDR subsides (32, 42).”
§ Aging, Cellular Senescence, and Cancer > SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE > The SASP: Regulation
What the sources say
- Partly supportedcites [32] sourceExperimental — accuracy not yet measured
The irradiation experiment (Figure 1D; page unavailable) reports that a robust SASP appeared 4–7 days after DNA damage, not immediately, and that both radiation doses initiated a DDR while only the senescence-inducing dose produced a SASP. The DDR discussion likewise calls the SASP a slow response rather than a simple or classic DDR. Neither passage establishes that the initial DDR had subsided before the SASP developed. (LLM, conf=0.86)
- Partly supportedcites [42] sourceExperimental — accuracy not yet measured
In the indexed passage labeled Abstract (page unavailable), the paper reports that IL-6 and IL-8 secretion rises over 2–5 days after high-dose irradiation, rather than immediately, and links the response to persistent DNA-damage signalling. It does not establish that the SASP begins only after the initial DDR subsides; it says DDR signalling persists and helps initiate the delayed cytokine response. (LLM, conf=0.86)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The SASP cytokines that are responsible for these immune responses are incompletely understood but are very likely numerous (132, 135).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: THE BRIGHT SIDE > Immune Clearance
What the sources say
- Partly supportedcites [132] sourceExperimental — accuracy not yet measured
The passage labeled Abstract (page not provided) reports that four inflammatory cytokines were upregulated after p53 reactivation in murine liver tumours, alongside infiltration by several innate immune cell types. This supports the suggestion that multiple cytokines may be involved, but the paper does not identify which cytokines are responsible for the immune responses or explicitly assess how completely they are understood. (LLM, conf=0.84)
- Partly supportedcites [135] sourceExperimental — accuracy not yet measured
The Abstract says IL-6, IL-8, and other secreted factors attract immune cells, and the ‘NF-kB controls the SASP’ section identifies multiple immune-response genes. This supports the involvement of several SASP factors, but the paper does not establish that numerous cytokines are responsible for the immune responses or explicitly say that their identities are incompletely understood. Its statement that little is known concerns regulation of the SASP, not which cytokines mediate immunity. (LLM, conf=0.82)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“There are also age-related changes in the innate immune system, although they tend to be less striking than the changes in adaptive immunity; moreover, the aged innate immune system is more likely to show a loss of proper regulation than a loss of function (142, 143).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: THE BRIGHT SIDE > Immune Clearance
What the sources say
- Partly supportedcites [142] sourceExperimental — accuracy not yet measured
The Abstract states that age-related innate immunosenescence appears to reflect dysregulation rather than exclusively impaired function, and the Introduction describes both diminished responses and hyper-reactivity. Neither passage establishes the claim that age-related innate changes are less striking than changes in adaptive immunity. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [143] source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Likewise, secreted WNT16B is an important enforcer of the senescence growth arrest of human fibroblasts in culture, as well as that of mouse cells that senesce in vivo owing to expression of an activated RAS oncogene (138).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: THE BRIGHT SIDE > Tumor Suppression
What the sources say
- Partly supportedcites [138] sourceExperimental — accuracy not yet measured
The Results section, “WNT16B is necessary for the onset of replicative senescence” (page unavailable), reports that WNT16B knockdown let cultured human fibroblasts bypass senescence and continue proliferating. The Results section, “WNT16 is activated in OIS in vitro and in vivo” (page unavailable), finds WNT16B overexpressed in activated-K-Ras mouse lung lesions, but identifies it there as a marker; it does not show that WNT16B enforces growth arrest in those mouse cells. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This signaling cascade induced both a senescence growth arrest and the expression of several genes that encode SASP proteins.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: THE BRIGHT SIDE > Tissue Repair
What the sources say
- Supportedcites [149] source
The Results section (“CCN1 induces senescence in human fibroblasts through integrin signaling”; page not provided) reports that CCN1 caused irreversible growth arrest in skin fibroblasts and increased expression of cytokine and matrix-degrading-enzyme genes consistent with the SASP. The Results section on ROS-dependent ERK and p38 MAPK activation links the signaling pathway to cellular senescence. (LLM, conf=0.91)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Supported
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer.”
§ Aging, Cellular Senescence, and Cancer > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Cellular senescence is unlikely to explain all aging phenotypes.”
§ Aging, Cellular Senescence, and Cancer > INTRODUCTION: AGING AND CANCER
hedged- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Among multicellular organisms, aging is marked by a progressive decline in the function of multiple cells and tissues.”
§ Aging, Cellular Senescence, and Cancer > INTRODUCTION: AGING AND CANCER
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The senescence response is widely recognized as a potent tumor suppressive mechanism.”
§ Aging, Cellular Senescence, and Cancer > Abstract
boosteddirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“Cellular senescence refers to the essentially irreversible arrest of cell proliferation (growth) that occurs when cells experience potentially oncogenic stress (8) (Figure 1).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: OVERVIEW
What the sources say
- Not checked — no full text of the sourcecites [8] source
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
In the paper
“Extrinsic hazards—accidents, predation, infection, starvation, and so forth—limit the life span of most species, thereby depleting natural populations of older individuals.”
§ Aging, Cellular Senescence, and Cancer > INTRODUCTION: AGING AND CANCER
What the sources say
- Not checked — no full text of the sourcecites [1] Rose MR, 1991 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“These changes include the secretion of numerous proinflammatory cytokines, chemokines, growth factors, and proteases, a feature termed the senescence-associated secretory phenotype (SASP) (Figures 2 and 3).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: OVERVIEW
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As discussed below, DDR signaling also establishes and maintains the SASP.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES > Telomere Shortening
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Telomerase-positive human cells include most cancer cells, embryonic stem cells, certain adult stem cells, and a few somatic cells (for example, activated T cells).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES > Telomere Shortening
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Because polymerases that copy DNA templates are unidirectional and require a labile primer, the ends of linear DNA molecules cannot be completely replicated (13).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES > Telomere Shortening
What the sources say
- Not checked — no full text of the sourcecites [13] source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Finally, the SASP is a plastic phenotype. That is, proteins that are included in the SASP vary among cell types and, to some extent, with the stimulus that induced the senescence response.”
§ Aging, Cellular Senescence, and Cancer > SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These cells were said to have a finite replicative life span, and, later, to undergo replicative or cellular senescence (sometimes termed replicative or cellular aging).”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The ensuing decades have seen the links between cellular senescence and both aging and cancer strengthen.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The link to cancer was more obvious.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Rather, cellular senescence and the SASP likely evolved both to suppress the development of cancer and to promote tissue repair or regeneration in the face of injury.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: OVERVIEW
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“They have also seen an increasingly more complex view of both the causes and consequences of cellular senescence.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: CAUSES
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“These proteins act upstream of p53, which does not positively regulate the SASP (discussed below) (Figure 2).”
§ Aging, Cellular Senescence, and Cancer > SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE > The SASP: Regulation
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The picture that emerges, then, is that senescent cells accumulate with age, creating a tissue microenvironment that is permissive for the development, or at least the progression, of cancer.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE, AGING, AND CANCER: THE DARK SIDE > Senescent Cells and Cancer
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“After all, cells enter a senescent state to prevent the proliferation of damaged cells, which is a major risk factor for the development of cancer.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE, AGING, AND CANCER: THE DARK SIDE > Senescent Cells and Cancer
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Of particular importance in this regard are the SASP components MMP3 (stromelysin) (130), which also promotes tumor cell invasion, and VEGF (97), which promotes tumor-driven angiogenesis.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE, AGING, AND CANCER: THE DARK SIDE > Senescent Cells and Cancer
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, in addition to suppressing tumorigenesis by implementing a cell-autonomous growth arrest, senescent cells can suppress cancer nonautonomously by stimulating the immune system to target oncogene-expressing premalignant or malignant cells.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: THE BRIGHT SIDE > Immune Clearance
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“This morphological transition enables transformed epithelial cells to invade and migrate through tissues and is critical in the development of metastatic cancer.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE, AGING, AND CANCER: THE DARK SIDE > Senescent Cells and Cancer
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The effects of senescent cells within the tumor microenvironment are complex and highly dependent on physiological context.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE, AGING, AND CANCER: THE DARK SIDE > Senescent Cells and Cancer
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The beneficial effect of senescent cells on tissue repair poses a paradox because wound healing and tissue repair decline with age.”
§ Aging, Cellular Senescence, and Cancer > RESOLVING THE PARADOXES
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Wound healing and tissue repair decline with age.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In both cases, senescent cells are not chronically present, which is the case during aging and at the sites of age-related pathologies.”
§ Aging, Cellular Senescence, and Cancer > RESOLVING THE PARADOXES
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The authors state this as an assumption.
Cells that express p16INK4a are senescent.
“there is strong evidence that p16INK4a-expressing cells are senescent, but this assumption has not yet been rigorously tested.”
The paper relies on this without support.
Wound healing and tissue repair decline with age.
“wound healing and tissue repair decline with age.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“During the early phases of cancer progression, mutated cells display a genuine senescent phenotype, as a consequence of oncogene-induced senescence150.”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [150]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“These senescent cells exhibit an altered secretome known as SASP, which significantly disrupts the skin microenvironment.158”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [158]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Oxidative stress and macromolecular damage in aged cells induce a complex stress response termed cellular senescence, which has been shown to cause or exacerbate aging and several age-related pathologies”
From Single-cell RNA sequencing identifies senescent cerebromicrovascular endothelial cells in the aged mouse brain (2020) · cites this paper as Campisi 2013
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Therefore, cellular senescence is believed to be an essential tumor suppression mechanism in vivo.”
From Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer (2020) · cites this paper as [1]
The cited source says what the claim attributes to it.
In the citing paper
“Senescent cells (SnCs) accumulate in many vertebrate tissues with age and contribute to age-related pathologies1–3, presumably through their secretion of factors contributing to the senescence-associated secretory phenotype (SASP)4–6.”
From Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment (2017) · cites this paper as [1]
The cited source says what the claim attributes to it.
In the citing paper
“The induction of cellular senescence is mediated by either Rb or p53, two critical tumor suppressors, and represents a potent anti-tumor mechanism (Campisi, 2013).”
From Single senescent cell sequencing reveals heterogeneity in senescent cells induced by telomere erosion (2019) · cites this paper as Campisi, 2013
The cited source says what the claim attributes to it.
In the citing paper
“the SASP does not depend on either p53 or p16INK4a, which suggests that it is controlled by an independent branch of the senescence regulatory network (2, 10, 20, 26).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [2]
The cited source says what the claim attributes to it.
In the citing paper
“factors secreted by senescent cells may directly or indirectly promote chronic inflammation that is thought to be a major factor in many, if not all, age-related diseases (2, 9, 10).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [2]
The cited source says what the claim attributes to it.
In the citing paper
“they also secrete inflammatory and other factors that can disrupt normal cellular functions, damage tissues and promote carcinogenesis61,62.”
From Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages (2020) · cites this paper as [62]
The cited source says what the claim attributes to it.
In the citing paper
“Senescence is a protective mechanism that induces cell cycle arrest to prevent transmission of defects to progeny cells, particularly to stop malignant transformation 72-74 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [73]
The cited source says what the claim attributes to it.
In the citing paper
“There is growing evidence that senescent cells and their SASPs contribute to the pathogenesis of many other age-related diseases as well”
From Single-cell RNA sequencing identifies senescent cerebromicrovascular endothelial cells in the aged mouse brain (2020) · cites this paper as Campisi 2013
The cited source says what the claim attributes to it.
In the citing paper
“Senescence is triggered by stressors such as telomere shortening, DNA damage, oxidative stress, and oncogenic signals5,6,7,8”
From Cellular senescence in human liver under normal aging and cancer (2026) · cites this paper as [6]
The cited source says what the claim attributes to it.
In the citing paper
“While chemotherapy can induce senescence in healthy tissues,6 it remains unclear whether metastatic cancer itself triggers senescence in adjacent normal liver and how this differs from aging.”
From Cellular senescence in human liver under normal aging and cancer (2026) · cites this paper as [6]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Clearance had no impact on the spectrum or incidence of postmortem tumors, which is consistent with the hypothesis that senescent cells help create a tissue microenvironment that promotes tumor progression 1 .”
From Naturally occurring p16Ink4a-positive cells shorten healthy lifespan (2016) · cites this paper as [1]
Experimental — accuracy not yet measuredIn the citing paper
“p21 and p16 are cyclin-dependent kinase inhibitors involved in preventing cell cycle progression by preventing pRB phosphorylation [37], [240].”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [240]
In the citing paper
“senescent cells display extensive changes in gene expression, including the expression and secretion of many proinflammatory cytokines, chemokines, growth factors, and proteases; collectively these features are termed the senescence-associated secretory phenotype (SASP) (2, 7–10).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [2]
In the citing paper
“the accumulation of senescent cells as organisms age is thought to promote aging-related phenotypes and aging-associated diseases, including cancer and neurodegeneration, in a cell-nonautonomous manner (2, 3, 10).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [2]
In the citing paper
“In particular, this failsafe cellular senescence reportedly occurs in response to (1) potentially carcinogenic events including oncogene activation or oncosuppressor gene inactivation; and (2) several sublethal cellular insults, including telomere shortening, DNA damage, mitochondrial dysfunction, defective/stalled DNA replication and epigenetic, lysosomal, mechanical, metabolic, mitotic, ox”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [933]
In the citing paper
“Among the known endogenous causes of this phenotype are DNA damage, dysfunctional telomeres, epigenomic disruption, mitogenic signals and oxidative stress56.”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [56]
In the citing paper
“Cellular stress induced by persistent DDR is a central mechanism that drives senescence in aging and age‐related diseases”
From p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling (2017) · cites this paper as Campisi, 2013
In the citing paper
“The accumulation of cells expressing a senescence-associated secretory phenotype (Campisi 2013; Young and Narita 2009) in different tissues, possibly induced by age-related NF-kB dysregulation (Bektas and others 2013), may also be a possible cause.”
From Gene expression markers of age-related inflammation in two human cohorts (2015) · cites this paper as Campisi 2013
In the citing paper
“A persistent DNA damage response (DDR) is the most unified pathway leading to senescence, with sensing by the Ataxia Telangiectasia Mutated (ATM) protein leading to p53 phosphorylation and upregulation of cell cycle inhibitors 72-74 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [73]
In the citing paper
“The risk for aging-associated outgrowth of cancerous cells is curbed through the cellular senescence program, which forces cells that have undergone repetitive replications into permanent cell cycle arrest [33].”
From T-cell aging in rheumatoid arthritis (2014) · cites this paper as [33]
In the citing paper
“Senescent cells increase with age in human and mouse tissues (Campisi, 2013; Wiley and Campisi, 2016)”
From Oxylipin biosynthesis reinforces cellular senescence and allows detection of senolysis (2021) · cites this paper as Campisi, 2013
In the citing paper
“The senescence-associated secretory phenotype (SASP) mediates the diverse functionality of senescent cells in an autocrine and paracrine manner”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [5]
In the citing paper
“the senescence response can have profound cell autonomous and non-cell autonomous activities in vivo 5,6 .”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [5]
In the citing paper
“On the other hand, senescent fibroblasts can influence their local environment by turning into proinflammatory cells that can promote the growth of transformed or preneoplastic neighboring epithelial cells in culture and in vivo [22,23,24].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [24]
In the citing paper
“SASP effects are beneficial or detrimental depending on the cell type, senescence stimulus, and the neighboring environment [24].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [24]
In the citing paper
“Despite these caveats, there is considerable evidence that senescent cells secrete cytokines that attract immune cells and lead to tumor clearance, providing a potential explanation for tumor regression (79).”
From Targeting CDK4 and CDK6: From Discovery to Therapy (2016) · cites this paper as [79]
In the citing paper
“Nevertheless, the incidence of cancer increases when people get older because of the increased burden of cell senescence in organs, partly due to an impaired immune system, which results in a reduced clearance of senescent cells.4”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [4]
In the citing paper
“One major hallmark of aging is the chronic accumulation of cellular senescence, a permanent state of cell-cycle arrest in response to various damaging stimuli.3,4”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [3]
In the citing paper
“However, the deleterious consequences that result from ineffective clearance of senescent cells and their over-accumulation in tissues can promote age-related diseases and cancer.2,26–30”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [27]
In the citing paper
“Supporting this notion, the burden of senescent cells in tissues increases significantly with age in mice, primates, and humans,27 and they can be found in both benign and malignant tumours.31–35”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [27]
In the citing paper
“A large number of proangiogenic factors are also known to be secreted by senescent cells, whereas angiostatic molecules have not been found to be secreted.27,60”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [27]
In the citing paper
“Furthermore, studies have shown that senescent cells are implicated in the genesis of age-related diseases such as AD and atherosclerosis [1].”
From Oxidative Stress and Ageing: The Influence of Environmental Pollution, Sunlight and Diet on Skin (2017) · cites this paper as [1]
In the citing paper
“Cellular senescence refers to the irreversible arrest of proliferation, which acts as a tumour-suppressive mechanism to inhibit cells with potentially cancerous mutations from undergoing replication [1].”
From Oxidative Stress and Ageing: The Influence of Environmental Pollution, Sunlight and Diet on Skin (2017) · cites this paper as [1]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: THE BRIGHT SIDE > Tumor Suppression
“Together, these findings support the idea that, at least for some factors and under some circumstances, the SASP helps maintain the tumor suppressive growth arrest of senescent cells.”
§ Aging, Cellular Senescence, and Cancer > CELLULAR SENESCENCE: THE BRIGHT SIDE > Tumor Suppression
“In these cases, the SASP components appear to help establish the senescence growth arrest, rather than maintain the arrest once it is fully established.”
Citations
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The serial cultivation of human diploid cell strains
Hayflick, L., & Moorhead, P. S. (1961) · Experimental Cell Research · doi:10.1016/0014-4827(61)90192-6 · Cited by 8,508
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
Dimri, G. P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens, M., Rubelj, I., & Pereira-Smith, O. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.20.9363 · Cited by 7,477
The limited in vitro lifetime of human diploid cell strains
Hayflick, L. (1965) · Experimental Cell Research · doi:10.1016/0014-4827(65)90211-9 · Cited by 5,876
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 1×
“The first report of what is now termed oncogene-induced senescence showed that an oncogenic form of H-RAS (H-RASV12), which chronically stimulates the mitogen-activated protein kinase (MAPK) signaling pathway, provokes senescence in normal cells (45).”
BackgroundThe senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
Self-citationCellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
Self-citationPleiotropy, natural selection, and the evolution of senescence.
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Items 301–400 of 2,942
The aging-disease false dichotomy: understanding senescence as pathology
Gems, D. (2015) · Frontiers in Genetics · doi:10.3389/fgene.2015.00212 · Cited by 136
“Here a snag is that our understanding of the biology of aging remains embryonic, though much progress has been made in recent decades (Blagosklonny, 2008; Kenyon, 2010; Bartke et al., 2013; Campisi, 2013; Vijg and Suh, 2013).”
BackgroundSenescent cells: Living or dying is a matter of NK cells
Antonangeli, F., Zingoni, A., Soriani, A., & Santoni, A. (2019) · Journal of Leukocyte Biology · doi:10.1002/jlb.mr0718-299r · Cited by 134
Lesina, M., Wörmann, S. M., Morton, J. P., Diakopoulos, K. N., Korneeva, O., Wimmer, M., Einwächter, H., Sperveslage, J., Demir, İ. E., Kehl, T., et al. (2016) · Journal of Clinical Investigation · doi:10.1172/jci86477 · Cited by 134
“In contrast, overexpression of the human ortholog of IL-8 inhibited progression of preneoplastic lesions through expansion of senescent mPanIN lesions (25).”
BackgroundIrizar, P. A., Schäuble, S., Esser, D., Groth, M., Frahm, C., Priebe, S., Baumgart, M., Hartmann, N., Marthandan, S., Menzel, U., et al. (2018) · Nature Communications · doi:10.1038/s41467-017-02395-2 · Cited by 127
Epithelial innate immunity mediates tubular cell senescence after kidney injury
Jin, H., Zhang, Y., Ding, Q. J., Wang, S., Rastogi, P., Dai, D., Lu, D., Purvis, M., Cao, C., Wang, A. Y., et al. (2019) · JCI Insight · doi:10.1172/jci.insight.125490 · Cited by 133
Self-citationMolecular Mechanisms Determining Lifespan in Short- and Long-Lived Species
Tian, X., Seluanov, A., & Gorbunova, V. A. (2017) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2017.07.004 · Cited by 130
Regulation of cellular senescence by extracellular matrix during chronic fibrotic diseases
Blokland, K. E. C., Pouwels, S. D., Schuliga, M. J., Knight, D. A., & Burgess, J. K. (2020) · Clinical Science · doi:10.1042/cs20190893 · Cited by 132
DNA Methylation Patterns Separate Senescence from Transformation Potential and Indicate Cancer Risk
Xie, W., Kagiampakis, I., Pan, L., Zhang, Y. W., Murphy, L., Tao, Y., Kong, X., Kang, B., Xia, L., Carvalho, F. L. F., et al. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.01.008 · Cited by 122
“, 2010), and senescence is well characterized to be related to aging (Campisi, 2013; van Deursen, 2014).”
Cell Autonomous and non-autonomous effects of senescent cells in the skin
Demaria, M., Desprez, P. Y., Campisi, J., & Velarde, M. C. (2015) · Journal of Investigative Dermatology · doi:10.1038/jid.2015.108 · Cited by 127
“Cellular senescence is a complex stress response that renders cells incapable of cell division, even in the presence of growth stimuli (Campisi, 2013).”
BackgroundInfluentialTherapeutics in Osteoarthritis Based on an Understanding of Its Molecular Pathogenesis
Kim, J., Yoo, J. J., & Kim, H. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19030674 · Cited by 139
Chemical screen identifies a geroprotective role of quercetin in premature aging
Geng, L., Liu, Z., Zhang, W., Li, W., Wu, Z., Wang, W., Ren, R., Su, Y., Wang, P., Sun, L., et al. (2018) · Protein & Cell · doi:10.1007/s13238-018-0567-y · Cited by 131
“…decline over time at cellular, tissue and organismal levels, leading to increased vulnerability to diseases that include cancer, neurodegenerative disorders, as well as cardiovascular and metabolic diseases (Benayoun et al., 2015; Campisi, 2013; Kudlow et al., 2007; López-Otín et al., 2013).”
BackgroundProtective Role of Melatonin and Its Metabolites in Skin Aging
Bocheva, G., Slominski, R. M., Janjetović, Z., Kim, T., Böhm, M., Steinbrink, K., Reiter, R. J., Kleszczyński, K., & Slominski, A. T. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23031238 · Cited by 139
“Chronic exposure can also cause an impairment of the epidermal barrier function [87] and alterations in the skin microbiome [88], leading to significant morbidity [70,89].”
BackgroundAge-driven developmental drift in the pathogenesis of idiopathic pulmonary fibrosis
Selman, M., López-Otín, C., & Pardo, A. (2016) · European Respiratory Journal · doi:10.1183/13993003.00398-2016 · Cited by 122
Age- and tissue-specific expression of senescence biomarkers in mice.
Hudgins, A. D., Tazearslan, C., Tare, A., Zhu, Y., Huffman, D., & Suh, Y. (2018) · Frontiers in Genetics · doi:10.3389/fgene.2018.00059 · Cited by 124
“These changes include alterations to chromatin organization, gene expression, and secretory profiles (Campisi, 2013).”
BackgroundmTOR Signaling from Cellular Senescence to Organismal Aging
Xu, S. (2014) · Aging and Disease · doi:10.14336/ad.2014.0500263 · Cited by 125
“However, emerging data show that these two cellular processes are linked together [48, 49].”
Pan, J., 宁波大学农产品质量安全危害因子与风险防控国家重点实验室, 浙. 宁. 3., Fei, C.-J., Hu, Y., Wu, X., Nie, L., Chen, J., 宁波大学梅山校区海洋学院生物化学与分子生物学实验室, 浙. 宁. 3., & 浙江省海洋生物工程重点实验室, 浙. 宁. 3. (2023) · 动物学研究 · doi:10.24272/j.issn.2095-8137.2022.464 · Cited by 138
“It acts as a natural tumor-prevention barrier and is also involved in fibrosis and tissue healing (Campisi, 2013).”
BackgroundExposome and unhealthy aging: environmental drivers from air pollution to occupational exposures
Pándics, T., Major, D., Fazekas‐Pongor, V., Szarvas, Z., Péterfi, A., Mukli, P., Gulej, R., Ungvari, A., Fekete, M., Tompa, A., et al. (2023) · GeroScience · doi:10.1007/s11357-023-00913-3 · Cited by 137
“Importantly, there is evidence that the inflammatory milieu maintained by senescent cells contribute to the development of metastases [332–336].”
BackgroundMouse Models to Disentangle the Hallmarks of Human Aging
Folgueras, A. R., Freitas-Rodríguez, S., Velasco, G., & López-Otín, C. (2018) · Circulation Research · doi:10.1161/circresaha.118.312204 · Cited by 113
“On senescence induction, cells secrete numerous proinflammatory cytokines, growth factors, and matrix remodeling enzymes that constitute the so called senescence-associated secretory phenotype.(175) In a conciliatory model, senescent cells might contribute to clear damage cells within a tissue through the recruitment…”
BackgroundSimvastatin suppresses breast cancer cell proliferation induced by senescent cells
Liu, S., Uppal, H., Demaria, M., Desprez, P.-Y., Campisi, J., & Kapahi, P. (2015) · Scientific Reports · doi:10.1038/srep17895 · Cited by 124
Self-citationMouse aging cell atlas analysis reveals global and cell type-specific aging signatures
Zhang, M. J., Pisco, A. O., Darmanis, S., & Zou, J. (2021) · eLife · doi:10.7554/elife.62293 · Cited by 121
Dysregulated Signalling Pathways Driving Anticancer Drug Resistance
Antoun, N. B., & Chioni, A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241512222 · Cited by 141
“As a tumour suppressor, the protein p16INK4a (also known as p16) inhibits the activity of cyclindependent kinases (CDKs) and slows cell division by delaying the transition from the G1 to the S phases of the cell cycle [124].”
BackgroundKang, C. (2019) · Europe PMC (PubMed Central) · doi:10.14348/molcells.2019.0298 · Cited by 129
“Advanced age steeply increases the risk for developing cancer, cardiovascular disease, neurodegenerative disorders, osteoporosis, osteoarthritis, and metabolic syndrome (Campisi, 2013; Childs et al., 2015; Munoz-Espin and Serrano, 2014).”
BackgroundDeterioration of nuclear morphology and architecture: A hallmark of senescence and aging
Pathak, R. U., Soujanya, M., & Mishra, R. K. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101264 · Cited by 126
Mechanisms of Radiation Toxicity in Transformed and Non-Transformed Cells
Panganiban, R. A. M., Snow, A. L., & Day, R. M. (2013) · International Journal of Molecular Sciences · doi:10.3390/ijms140815931 · Cited by 131
“IR- or chemotherapy-induced pathologies [36,162,164].”
BackgroundInfluentialCellular senescence, senescence-associated secretory phenotype, and chronic kidney disease
Wang, W.-J., Cai, G.-Y., & Chen, X.-M. (2017) · Oncotarget · doi:10.18632/oncotarget.17327 · Cited by 121
“The DDR, in turn, arrests cell division primarily through activation of the p53/p21 and p16INK4a/retinoblastoma (Rb) pathways, thereby preventing genomic instability, enforcing senescence growth arrest, and establishing and maintaining SASP [59, 65, 66].”
BackgroundStressing the cell cycle in senescence and aging
Chandler, H., & Peters, G. (2013) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2013.07.005 · Cited by 119
Extracellular Vesicles as New Players in Cellular Senescence
Urbanelli, L., Buratta, S., Sagini, K., Tancini, B., & Emiliani, C. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17091408 · Cited by 126
“Therefore, it represents a barrier towards neoplastic lesions [3].”
BackgroundSocial stress shortens lifespan in mice
Razzoli, M., Nyuyki, K. D., Gurney, A., Erickson, C., McCallum, J., Spielman, N., Marzullo, M., Patricelli, J., Kurata, M., Pope, E. A., et al. (2018) · Aging Cell · doi:10.1111/acel.12778 · Cited by 119
“Given the known association between cellular senescence, cancer, and aging (Campisi, 2013), we asked whether the difference in social status during the LCPS led to differences in cancer prevalence that might underlie the survival effect.”
BackgroundThe Impact of Vitamin D on Skin Aging
Bocheva, G., Slominski, R. M., & Slominski, A. T. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22169097 · Cited by 134
Cellular senescence and cardiovascular diseases: moving to the “heart” of the problem
Evangelou, K., Vasileiou, P. V. S., Papaspyropoulos, A., Hazapis, O. G., Petty, R., Demaria, M., & Gorgoulis, V. G. (2022) · Physiological Reviews · doi:10.1152/physrev.00007.2022 · Cited by 127
The Role of Oxidative Stress in Tumorigenesis and Progression
Li, K., Deng, Z., Lei, C., Ding, X., Li, J., & Wang, C. (2024) · Cells · doi:10.3390/cells13050441 · Cited by 142
“SASP promotes malignant phenotypes in nearby cells [105] and formats the tumor-permissive microenvironment [117].”
BackgroundLi, C., Xie, N., Li, Y., Liu, C., Hou, F. F., & Wang, J. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.11.006 · Cited by 121
Cellular senescence in lung cancer: Molecular mechanisms and therapeutic interventions
Jha, S. K., Rubis, G. D., Devkota, S. R., Zhang, Y., Adhikari, R., Jha, L. A., Bhattacharya, K., Mehndiratta, S., Gupta, G., Singh, S. K., et al. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102315 · Cited by 138
“Lipofuscin accumulates in the lysosomes of cells undergoing senescence because of age-related lysosomal dysfunction (Campisi, 2013; Gorgoulis et al., 2019; Hernandez-Segura et al., 2018).”
Osteocyte RANKL is required for cortical bone loss with age and is induced by senescence
Kim, H.-N., Xiong, J., MacLeod, R. S., Iyer, S., Fujiwara, Y., Cawley, K. M., Han, L., He, Y., Thostenson, J. D., Ferreira, E., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.138815 · Cited by 117
“SASP factors reinforce growth arrest in an autocrine manner and alter the behavior of surrounding cells in a paracrine manner (10–12).”
BackgroundInfluentialBaicalein and baicalin inhibit colon cancer using two distinct fashions of apoptosis and senescence
Dou, J., Wang, Z., Ma, L., Peng, B., Mao, K., Li, C., Su, M., Zhou, C., & Peng, G. (2018) · Oncotarget · doi:10.18632/oncotarget.24015 · Cited by 123
“In addition to the most somatic cells undergoing aging or infected with age-related pathologies [29], cellular senescence is now thought to be a tumor suppressive mechanism that could be harnessed for cancer therapy [26, 30].”
BackgroundIonizing radiation-induced cellular senescence promotes tissue fibrosis after radiotherapy. A review
Nguyen, H. Q., To, N. H., Zadigue, P., Kerbrat, S., TAILLE, A. D. L., Gouvello, S. L., & Belkacémi, Y. (2018) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2018.06.012 · Cited by 129
Epigenetics in Cardiac Fibrosis
Felisbino, M. B., & McKinsey, T. A. (2018) · JACC Basic to Translational Science · doi:10.1016/j.jacbts.2018.05.003 · Cited by 124
“Cellular senescence is an irreversible form of cell cycle arrest initially described as a consequence of replicative exhaustion and telomere erosion; however, it is now known that it can be triggered by various cellular stresses, including DNA damage, oncogene activation, and reactive oxygen species (117,118).”
BackgroundPeng, X., Wu, Y., Brouwer, U., van Vliet, T., Wang, B., Demaria, M., Barazzuol, L., & Coppes, R. P. (2020) · Cell Death and Disease · doi:10.1038/s41419-020-03074-9 · Cited by 126
Adipose Tissue Remodeling in Pathophysiology
Auger, C., & Kajimura, S. (2022) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-042220-023633 · Cited by 135
Song, C., Zhou, Y., Cheng, K., Liu, F., Cai, W., Zhou, D., Chen, R., Shi, H., Fu, Z., Chen, J., et al. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.114711 · Cited by 125
Lau, L., Porciuncula, A., Yu, A., Iwakura, Y., & David, G. (2019) · Molecular and Cellular Biology · doi:10.1128/mcb.00586-18 · Cited by 119
“This is consistent with the theory of antagonistic pleiotropy, where traits that are selected for early in life become harmful as organisms age (19).”
BackgroundThe role of estrogen deficiency in skin ageing and wound healing
Emmerson, E., & Hardman, M. J. (2012) · Biogerontology · doi:10.1007/s10522-011-9322-y · Cited by 118
SIRT1 ameliorates age-related senescence of mesenchymal stem cells via modulating telomere shelterin
Chen, H., Liu, X., Zhu, W., Chen, H., Hu, X., Jiang, Z., Xu, Y., Wang, L., Zhou, Y., Chen, P., et al. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00103 · Cited by 119
“Senescence-associated β-galactosidase (SA-β-gal) is universally accepted as a marker for senescent cells (Kuilman et al., 2010; Sikora et al., 2011; Campisi, 2013; Sikora, 2013).”
BackgroundMethodInfluentialOf Flies, Mice, and Men: Evolutionarily Conserved Tissue Damage Responses and Aging
Neves, J., Demaria, M., Campisi, J., & Jasper, H. (2015) · Developmental Cell · doi:10.1016/j.devcel.2014.11.028 · Cited by 119
Self-citationKim, C., Kang, D., Lee, E. K., & Lee, J. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/2062384 · Cited by 117
“Hayflick and Moorehead firstly described replicative senescence (RS), which is an exhaustion of replicative potential in human diploid fibroblasts after continuous cultivation [1, 2].”
BackgroundAging: Molecular Pathways and Implications on the Cardiovascular System
de Almeida, A. J. P. O., Ribeiro, T. P., & de Medeiros, I. A. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/7941563 · Cited by 120
“Morphologically, the senescent cells are characterized by the increase in volume, and if adherent, they adopt a flattened morphology; however, there is no marker exclusive to a senescent state [3].”
BackgroundBlock, T. J., Marinkovic, M., Tran, O. N., Gonzalez, A. O., Marshall, A., Dean, D. D., & Chen, X. (2017) · Stem Cell Research & Therapy · doi:10.1186/s13287-017-0688-x · Cited by 120
Radiation-induced astrocyte senescence is rescued by Δ133p53
Turnquist, C., Beck, J. A., Horikawa, I., Obiorah, I. E., Von Muhlinen, N., Vojtesek, B., Lane, D. P., Grunseich, C., Chahine, J. J., Ames, H. M., et al. (2019) · Neuro-Oncology · doi:10.1093/neuonc/noz001 · Cited by 118
Transposable elements in mammalian chromatin organization
Lawson, H. A., Liang, Y., & Wang, T. (2023) · Nature Reviews Genetics · doi:10.1038/s41576-023-00609-6 · Cited by 124
Paramos-de-Carvalho, D., Jacinto, A., & Saúde, L. (2021) · eLife · doi:10.7554/elife.72449 · Cited by 111
“Aging entails a progressive loss of tissue functions that eventually leads to several chronic and agerelated diseases (Campisi, 2013).”
BackgroundThe “life code”: A theory that unifies the human life cycle and the origin of human tumors
Liu, J. (2019) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2019.09.005 · Cited by 120
Yabluchanskiy, A., Tarantini, S., Balasubramanian, P., Kiss, T., Csípő, T., Fülöp, G., Lipécz, Á., Ahire, C., DelFavero, J., Nyúl‐Tóth, Á., et al. (2020) · GeroScience · doi:10.1007/s11357-020-00154-8 · Cited by 124
“…contribute to the pathogenesis of many age-related diseases (Cohen and Torres 2019; Childs et al. 2016; Campisi 2016; Chinta et al. 2014; Tchkonia et al. 2013; Campisi 2013; Farr et al. 2017; Baker et al. 2011; Xu et al. 2018; Tchkonia and Kirkland 2018; Ogrodnik et al. 2018; Justice et al. 2018).”
BackgroundSelf-citationSystemic DNA damage responses in aging and diseases
Ribezzo, F., Shiloh, Y., & Schumacher, B. (2016) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2015.12.005 · Cited by 116
“Strikingly, cell senescence may lead to different outcomes – suppression of malignancy or acceleration of aging – depending on the context and persistence of senescent cells in vivo [88,90,91].”
Dynamics of Lung Defense in Pneumonia: Resistance, Resilience, and Remodeling
Quinton, L. J., & Mizgerd, J. P. (2014) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021014-071937 · Cited by 122
Cellular senescence: a promising strategy for cancer therapy
Lee, S., & Lee, J. (2019) · BMB Reports · doi:10.5483/bmbrep.2019.52.1.294 · Cited by 117
“Telomere erosion, the gradual loss of telomeres, has been generally accepted as the cause of RS (2, 3).”
BackgroundCancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment
Wang, S., Prizment, A. E., Thyagarajan, B., & Blaes, A. H. (2021) · Cancers · doi:10.3390/cancers13030427 · Cited by 118
Long noncoding RNAs in aging and age-related diseases
Kour, S., & Rath, P. C. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.12.001 · Cited by 123
Ucer, S., Iyer, S. V., Kim, H., Han, L., Rutlen, C., Allison, K. C., Thostenson, J. D., de Cabo, R., Jilka, R. L., O’Brien, C. A., et al. (2016) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.3014 · Cited by 123
“The effects of aging, on the other hand, result from a decline of osteoblast progenitors owing in part to mitochondrial dysfunction, ROS accumulation, and DNA damage, as well as increased osteoclastogenesis caused probably by other mechanisms of aging (independent of sex steroid deficiency), such as the senescence-ass…”
BackgroundObesity-induced cognitive impairment in older adults: a microvascular perspective
Balasubramanian, P., Kiss, T., Tarantini, S., Nyúl‐Tóth, Á., Ahire, C., Yabluchanskiy, A., Csípő, T., Lipécz, Á., Tabák, Á. G., Institóris, Á., et al. (2020) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00736.2020 · Cited by 116
“Senescent cells accumulate in various tissues of 473 the body including the brain during aging and have been implicated in the pathogenesis of age-related 474 diseases (16, 17, 41, 42, 53, 54, 61, 102, 145, 162, 293, 301).”
BackgroundComprehensive transcriptional landscape of aging mouse liver
White, R. R., Milholland, B., MacRae, S. L., Lin, M., Zheng, D., & Vijg, J. (2015) · BMC Genomics · doi:10.1186/s12864-015-2061-8 · Cited by 116
“5) link together genes shown to be highly important in aging such as Cdkn1a, Il6R, Mmp12, Top2a, Pdgfc, Lama3, and E2f1 [45–47].”
BackgroundImpact of ERK5 on the Hallmarks of Cancer
Stecca, B. A., & Rovida, E. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20061426 · Cited by 114
“On the other hand, cellular senescence, characterized by an irreversible arrest in cell proliferation, is among the biological processes that may prevent cellular immortality [74].”
BackgroundAquino-Martinez, R., Rowsey, J. L., Fraser, D. G., Eckhardt, B. A., Khosla, S., Farr, J. N., & Monroe, D. G. (2020) · Bone · doi:10.1016/j.bone.2019.115220 · Cited by 114
“In addition to replicative senescence, which is associated with aging phenotypes, stressinduced senescence is also observed following persistent DNA damage resulting from oncogenic or oxidative stress [6, 7].”
BackgroundThe Paradoxical Role of Cellular Senescence in Cancer
Yang, J., Liu, M., Hong, D., Zeng, M., & Zhang, X. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.722205 · Cited by 125
“Furthermore, senescent cells exhibit flattened morphology with a prominent nucleus and increased cytoplasmic granularity (Cadenas et al., 2012; Campisi, 2013).”
BackgroundSystemic induction of senescence in young mice after single heterochronic blood exchange
Jeon, O. H., Mehdipour, M., Gil, T.-H., Kang, M., Aguirre, N. W., Robinson, Z. R., Kato, C., Etienne, J., Lee, H. G., Alimirah, F., et al. (2022) · Nature Metabolism · doi:10.1038/s42255-022-00609-6 · Cited by 114
“1b), (2) up-regulated senescence-associated β-galactosidase (SA-β-gal) (Fig.”
Self-citationThe emerging role of senescent cells in tissue homeostasis and pathophysiology
Tominaga, K. (2015) · Pathobiology of Aging & Age-related Diseases · doi:10.3402/pba.v5.27743 · Cited by 117
“This is called senescence-associated secretory phenotype (SASP) (62) or senescence messaging secretome (SMS) (63).”
BackgroundAtaxia-telangiectasia (A-T): An emerging dimension of premature ageing
Shiloh, Y., & Lederman, H. M. (2016) · Ageing Research Reviews · doi:10.1016/j.arr.2016.05.002 · Cited by 115
Cellular senescence in the lung across the age spectrum
Parikh, P., Wicher, S., Khandalavala, K., Pabelick, C. M., Britt, R. D., & Prakash, Y. S. (2019) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00424.2018 · Cited by 112
“The concept of cellular senescence is most commonly associated with biological aging (31, 32, 33, 97, 168), and much exciting research has focused on understanding senescence pathways with a goal of blunting their effects and improving the healthspan of the elderly (95, 96, 136) (i.”
BackgroundCurrent Perspective in the Discovery of Anti-aging Agents from Natural Products
Ding, A., Zheng, S., Huang, X., Xing, T.-K., Wu, G.-S., Sun, H., Qi, S., & Luo, H. (2017) · Natural Products and Bioprospecting · doi:10.1007/s13659-017-0135-9 · Cited by 115
In vitro assays and techniques utilized in anticancer drug discovery
Ediriweera, M. K., Tennekoon, K. H., & Samarakoon, S. R. (2018) · Journal of Applied Toxicology · doi:10.1002/jat.3658 · Cited by 116
“Telomeres help to prevent uncontrolled cell proliferation and the absence of telomeres results in aneuploidy and cell death (Campisi, 2013; Van Deursen, 2014).”
BackgroundInfluentialAssociation of Metformin Use With Age-Related Macular Degeneration
Blitzer, A. L., Ham, S. A., Colby, K. A., & Skondra, D. (2021) · JAMA Ophthalmology · doi:10.1001/jamaophthalmol.2020.6331 · Cited by 117
The aging-related risk signature in colorectal cancer
Yue, T., Chen, S., Zhu, J., Guo, S., Huang, Z., Wang, P., Zuo, S., & Liu, Y. (2021) · Aging · doi:10.18632/aging.202589 · Cited by 116
“The major manifestations of aging are the gradual loss of function or degeneration at the molecular, cellular, tissue and body levels [4].”
BackgroundIncreased cell senescence in human metabolic disorders
Spinelli, R., Baboota, R. K., Gogg, S., Bèguinot, F., Blüher, M., Nerstedt, A., & Smith, U. (2023) · Journal of Clinical Investigation · doi:10.1172/jci169922 · Cited by 119
“Stress-induced premature senescence is caused by epigenetic changes, DNA damage, bioactive lipids, mitochondrial dysfunction, protein alterations, inflammatory mediators, and other danger signals (6, 19).”
White, R. R., Milholland, B., de Bruin, A., Curran, S., Laberge, R.-M., van Steeg, H., Campisi, J., Maslov, A. Y., & Vijg, J. (2015) · Nature Communications · doi:10.1038/ncomms7790 · Cited by 107
“…being a safeguard against cancer, might cause age-related degeneration not only through a decrease in mitotic potential, thereby reducing regenerative capability, but also through the secretion of inflammatory cytokines 54 , which can even promote hyperplastic growth in surrounding cells 47 .”
Self-citationMatsudaira, T., Nakano, S., Konishi, Y., Kawamoto, S., Uemura, K., Kondo, T., Sakurai, K., Ozawa, T., Hikida, T., Komine, O., et al. (2023) · Communications Biology · doi:10.1038/s42003-023-05027-2 · Cited by 98
“Accumulating evidence indicates that cellular senescence leads to a decline in tissue function, associated with ageing and various diseases 11,12 .”
Ladomersky, E., Zhai, L., Lauing, K. L., Bell, A., Xu, J., Kocherginsky, M., Zhang, B., Wu, J. D., Podojil, J. R., Platanias, L. C., et al. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-3874 · Cited by 110
“The most prominent feature of aging is a gradual loss of functional reserve that results in degeneration at the molecular, cellular, tissue, and organismal levels (40).”
BackgroundSelf-citationExpansion and Cell-Cycle Arrest: Common Denominators of Cellular Senescence
Ogrodnik, M., Salmonowicz, H., Jurk, D., & Passos, J. F. (2019) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2019.06.011 · Cited by 104
The Werner syndrome RECQ helicase targets G4 DNA in human cells to modulate transcription
Tang, W., Robles, A. I., Beyer, R. P., Gray, L. T., Nguyen, G. H., Oshima, J., Maizels, N., Harris, C. C., & Monnat, R. J. (2016) · Human Molecular Genetics · doi:10.1093/hmg/ddw079 · Cited by 109
“These pathways reflect known biochemical or functional activities of WRN (21,22,28) that when lost may affect genome stability, cell proliferation and the suppression of senescence (2,3,26,31).”
BackgroundHonegger, A., Leitz, J., Bulkescher, J., Hoppe‐Seyler, K., & Hoppe‐Seyler, F. (2013) · International Journal of Cancer · doi:10.1002/ijc.28164 · Cited by 108
“Activation of p53- and pRb-associated pathways is considered to play a major role in the regulation of senescence.(58) HPVs interfere with both pathways through the activity of the viral E6 and E7 oncoproteins,(3) and reactivation of p53 and pRb activities after E6/E7 inhibition is linked to senescence induction.”
BackgroundAutophagy and senescence in cancer therapy
Gewirtz, D. A. (2013) · Journal of Cellular Physiology · doi:10.1002/jcp.24420 · Cited by 110
Durso, D. F., Bacalini, M. G., Sala, C., Pirazzini, C., Marasco, E., Bonafè, M., do Valle, Í. F., Gentilini, D., Castellani, G., Faria, A. M. C., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.15573 · Cited by 108
Capasso, S., Alessio, N., Squillaro, T., Bernardo, G. D., Melone, M. A. B., Cipollaro, M., Peluso, G., & Galderisi, U. (2015) · Oncotarget · doi:10.18632/oncotarget.6277 · Cited by 108
“Dissecting molecular pathways underlying the multi-step progression of senescence and the onset of acute versus chronic senescent cells may trigger the discovery of new therapies for senescence-related diseases and aging [2, 3].”
BackgroundCell non-autonomous regulation of health and longevity
Miller, H. A., Dean, E. S., Pletcher, S. D., & Leiser, S. F. (2020) · eLife · doi:10.7554/elife.62659 · Cited by 102
“While the local effects of these signals have been well-studied, their systemic effects remain unclear (Campisi, 2013).”
BackgroundAbdul-Aziz, A. M., Sun, Y., Hellmich, C., Marlein, C. R., Mistry, J., Forde, E., Piddock, R. E., Shafat, M. S., Morfakis, A., Mehta, T., et al. (2019) · Blood · doi:10.1182/blood-2018-04-845420 · Cited by 105
Self-citationMandelblatt, J. S., Jacobsen, P. B., & Ahles, T. A. (2014) · Journal of Clinical Oncology · doi:10.1200/jco.2014.55.1259 · Cited by 106
“These senescent cells evoke inflammatory responses and accumulate at sites of pathology, including the brain.(20,21) Senescent cells can also be considered biomarkers of the frailty phenotype(22) that place patients with cancer at risk for cognitive impairment.”
BackgroundAnalysis of cancer genomes reveals basic features of human aging and its role in cancer development
Podolskiy, D. I., Lobanov, A. V., Kryukov, G. V., & Gladyshev, V. N. (2016) · Nature Communications · doi:10.1038/ncomms12157 · Cited by 100
“Since cancer is a disease of aging 8,9 , age-related changes in mutation accumulation also expose patterns of damage accumulation in cells 53 .”
CD58/CD2 Is the Primary Costimulatory Pathway in Human CD28−CD8+ T Cells
Leitner, J., Herndler-Brandstetter, D., Zlabinger, G. J., Grubeck-Loebenstein, B., & Steinberger, P. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1401917 · Cited by 104
Bektas, A., Schurman, S. H., Franceschi, C., & Ferrucci, L. (2020) · Immunity & Ageing · doi:10.1186/s12979-020-00196-8 · Cited by 102
Mahoney, S. A., Venkatasubramanian, R., Darrah, M. A., Ludwig, K. R., VanDongen, N. S., Greenberg, N., Longtine, A. G., Hutton, D. A., Brunt, V. E., Campisi, J., et al. (2023) · Aging Cell · doi:10.1111/acel.14060 · Cited by 111
“…healing and inhibits tumorigenesis in part through the production of the senescence-associated secretory phenotype (SASP)—a collection of cytokines, chemokines, and inflammatory mediators—which activate immune responses (Campisi, 2013; Campisi & d'Adda di Fagagna, 2007; Demaria et al., 2014 ).”
BackgroundSelf-citationInsects as models to study the epigenetic basis of disease
Mukherjee, K., Twyman, R. M., & Vilcinskas, A. (2015) · Progress in Biophysics and Molecular Biology · doi:10.1016/j.pbiomolbio.2015.02.009 · Cited by 107
“This affects cellular processes such as senescence (Campisi, 2013), telomere shortening (Kaszubowska, 2008), mTOR-dependent autophagy (Vellai et al., 2009), and the activity of Sirtuins, which are class III HDACs (Greiss and Gartner, 2009).”
BackgroundHiraoka, K., Inoue, T., Taylor, R. D., Watanabe, T., Koshikawa, N., Yoda, H., Shinohara, K., Takatori, A., Sugimoto, H., Maru, Y., et al. (2015) · Nature Communications · doi:10.1038/ncomms7706 · Cited by 103
Sangar, M. L. C., Genovesi, L. A., Nakamoto, M. W., Davis, M. J., Knobluagh, S. E., Ji, P., Millar, A., Wainwright, B. J., & Olson, J. M. (2017) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-2943 · Cited by 103
“Senescent cells release proinflammatory cytokines leading to elimination of tumor cells by phagocytosis (44).”
Cellular senescence and radiation-induced pulmonary fibrosis
He, Y., Thummuri, D., Zheng, G., Okunieff, P. G., Citrin, D. E., Vujašković, Ž., & Zhou, D. (2019) · Translational research · doi:10.1016/j.trsl.2019.03.006 · Cited by 107
Yentrapalli, R., Azimzadeh, O., Sriharshan, A., Malinowsky, K., Merl‐Pham, J., Wójcik, A., Harms‐Ringdahl, M., Atkinson, M. J., Becker, K., Haghdoost, S., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0070024 · Cited by 106
“Senescent cells remain metabolically active and generally adopt phenotypes including flattened cell morphology, altered gene and protein expression, and positive senescence-associated bgalactosidase (SA-ß-gal) staining [14].”
BackgroundHepatic senescence, the good and the bad
Huda, N., Liu, G., Hong, H., Yan, S., Khambu, B., & Yin, X.-M. (2019) · World Journal of Gastroenterology · doi:10.3748/wjg.v25.i34.5069 · Cited by 100
Regulation of lipids is central to replicative senescence
Lizardo, D. Y., Lin, Y., Gökçümen, Ö., & Atilla‐Gokcumen, G. E. (2017) · Molecular BioSystems · doi:10.1039/c6mb00842a · Cited by 102
Biophysical and biomolecular determination of cellular age in humans
Phillip, J. M., Wu, P.-H., Gilkes, D. M., Williams, W. A., McGovern, S., Daya, J., Chen, J., Aifuwa, I., Lee, J. S. H., Fan, R., et al. (2017) · Nature Biomedical Engineering · doi:10.1038/s41551-017-0093 · Cited by 106
miR-127 Regulates Cell Proliferation and Senescence by Targeting BCL6
Chen, J., Wang, M., Guo, M., Xie, Y., & Cong, Y. (2013) · PLoS ONE · doi:10.1371/journal.pone.0080266 · Cited by 102
“Cellular senescence causes permanent cell cycle arrest and, thereby, acts as a potent tumor suppression mechanism that prevents the oncogenic transformation of primary human cells [2,4].”
BackgroundChromatin basis of the senescence-associated secretory phenotype
Hao, X., Wang, C., & Zhang, R. (2022) · Trends in Cell Biology · doi:10.1016/j.tcb.2021.12.003 · Cited by 94
Cellular senescence and tumor promotion: Is aging the key?
Loaiza, N., & Demaria, M. (2016) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2016.01.007 · Cited by 101
Song, X., Narzt, M., Nagelreiter, I., Hohensinner, P. J., Terlecki‐Ζaniewicz, L., Tschachler, E., Grillari, J., & Грубер, Ф. (2016) · Redox Biology · doi:10.1016/j.redox.2016.12.015 · Cited by 105
“Cellular senescence withdraws the cells from the cell cycle and halts proliferation, and that allows repair of the damage over a longer timespan or the alerting of the immune system for clearance of the cell [45,46].”
Background
Metadata
- Authors
- Campisi, J.
- Affiliations
- Buck Institute for Research on Aging (US)
- Corresponding author
- Campisi, Judith
- ORCID
- Campisi, Judith
- Venue
- Annual Review of Physiology
- Publisher
- Annual Reviews
- Published
- 2013-02-10
- Volume
- 75
- Issue
- 1
- Pages
- 685-705
- ISSN
- 0066-4278 (ISSN-L)
- 1545-1585
- PMC
- PMC4166529
- OpenAlex
- W2150748567
- Semantic Scholar
- 06fb9247d328a192b4dc9451bbc06b9d7930f1b8
- Cited by
- 2,954
- References
- 152
- Citations by year
- 2026: 220 · 2025: 270 · 2024: 267 · 2023: 269 · 2022: 279 · 2021: 278 · 2020: 268 · 2019: 261 · 2018: 205 · 2017: 185 · 2016: 163 · 2015: 125 · 2014: 115 · 2013: 46
- FWCI
- 9.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Physiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R37AG009909, P01AG041122, P01AG017242)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cellular senescence, aging, cancer, tumor suppression, chronic inflammation, antagonistic pleiotropy, cellular stress response, malignant transformation
- MeSH terms
- Aging, Animals, Disease Models, Animal, DNA Damage, Humans, Neoplasms, Stress, Physiological, Cellular Senescence
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