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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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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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.
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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
“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.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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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
“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.
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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.
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.
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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 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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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.
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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.
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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
“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.
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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.
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- 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.
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- 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
“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
“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 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]
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
“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]
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
“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]
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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Immunity, Inflammation, and Cancer
Grivennikov, S. I., Greten, F. R., & Karin, M. (2010) · Cell · doi:10.1016/j.cell.2010.01.025 · Cited by 10,755
The serial cultivation of human diploid cell strains
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A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
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“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
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Strategic outline of interventions targeting extracellular matrix for promoting healthy longevity
Park, J. Y. C., King, A., Björk, V., English, B. W., Fedintsev, A., & Ewald, C. Y. (2023) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00060.2023 · Cited by 32
Ling, G., & Xu, C.-E. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1150304 · Cited by 25
“Multiple cellular stressors, including telomere shortening and DNA damage, drive cellular senescence, which is de fi ned by the irreversible cessation of the cell cycle (3).”
BackgroundSakai, C., Ueda, K., Goda, K., Fujita, R., Maeda, J., Nakayama, S., Sotomaru, Y., Tashiro, S., Yoshizumi, M., Ishida, T., et al. (2023) · Scientific Reports · doi:10.1038/s41598-023-43848-7 · Cited by 28
Maya‐Mendoza, A., Merchut‐Maya, J. M., Bártková, J., Bártek, J., Streuli, C. H., & Jackson, D. A. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.315 · Cited by 24
Shorter Ends, Faster End? Leukocyte Telomere Length and Mortality Among Older Taiwanese
Glei, D. A., Goldman, N., Weinstein, M., & Risques, R. A. (2014) · The Journals of Gerontology Series A · doi:10.1093/gerona/glu191 · Cited by 24
“Cell senescence is believed to contribute to aging (3), which has led to the hypothesis that telomere shortening has a causal effect on mortality.”
BackgroundAging with ING: a comparative study of different forms of stress induced premature senescence
Rajarajacholan, U. K., & Riabowol, K. T. (2015) · Oncotarget · doi:10.18632/oncotarget.5947 · Cited by 25
“Thus, understanding cell senescence would bridge our understanding of pathways governing both cancer and aging [3, 9, 10].”
BackgroundMitochondrial damage and ageing using skin as a model organ
Hudson, L., Bowman, A., Rashdan, E., & Birch-Machin, M. A. (2016) · Maturitas · doi:10.1016/j.maturitas.2016.04.021 · Cited by 25
“tissues of the body, leading to an increase in susceptibility to age-related diseases including cancer, and eventually the death of the organism [1].”
BackgroundLa, S.-H., Kim, S.-J., Kang, H.-G., Lee, H., & Chun, K. (2016) · Oncotarget · doi:10.18632/oncotarget.10986 · Cited by 24
“The permanence of senescence growth arrest enforces the senescence response and suppresses the development of cancer [14].”
BackgroundLompardía, S. L., Díaz, M., Papademetrio, D. L., Pibuel, M. A., Álvarez, É., & Hajos, S. E. (2016) · Investigational New Drugs · doi:10.1007/s10637-016-0397-9 · Cited by 25
Drug-induced premature senescence model in human dental follicle stem cells
Zhai, Y., Wei, R., Liu, J., Wang, H., Cai, W., Zhao, M., Hu, Y., Wang, S., Yang, T., Liu, X., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.14085 · Cited by 26
“Oppositely, genomic integrity which is maintained by DNA repair pathways may defer cell senescence and aging [10].”
BackgroundThe AKT/BCL-2 Axis Mediates Survival of Uterine Leiomyoma in a Novel 3D Spheroid Model
Vidimar, V., Chakravarti, D., Bulun, S. E., Yin, P., Nowak, R. A., Wei, J., & Kim, J. J. (2018) · Endocrinology · doi:10.1210/en.2017-03191 · Cited by 26
Interacting NAD + and Cell Senescence Pathways Complicate Antiaging Therapies
Mendelsohn, A. R., & Larrick, J. W. (2019) · Rejuvenation Research · doi:10.1089/rej.2019.2218 · Cited by 25
“15 Cell senescence is a complex phenomenon that seems to vary by tissue type and route of induction.”
The Therapeutic Potential of the Endocannabinoid System in Age-Related Diseases
Tudorancea, I. M., Ciorpac, M., Stanciu, G. D., Caratașu, C.-C., Săcărescu, A., Ignat, B. E., Burlui, A., Rezuş, E., Creangă-Murariu, I., Alexa‐Stratulat, T., et al. (2022) · Biomedicines · doi:10.3390/biomedicines10102492 · Cited by 28
“Aging involves degenerative processes and functional changes at molecular, cellular, tissue, and whole body levels [69,70].”
BackgroundAlessio, N., Aprile, D., Peluso, G., Mazzone, V., Patrone, D., Bernardo, G. D., & Galderisi, U. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01469-1 · Cited by 26
“The senescent executive program promotes cell cycle arrest, chromatin remodeling, the onset of senescence-related gene expression patterns, and the release of various factors collectively referred to as the senescence-specific associate phenotype (SASP) [1, 2].”
BackgroundGenetic origins, regulators, and biomarkers of cellular senescence
Torres, G., Salladay-Perez, I. A., Dhingra, A., & Covarrubias, A. J. (2024) · Trends in Genetics · doi:10.1016/j.tig.2024.08.007 · Cited by 24
Biological constraint, evolutionary spandrels and antagonistic pleiotropy
Gems, D., & Kern, C. C. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102527 · Cited by 36
“…cases decline (such as organ atrophy) is caused by active mechanisms, as where osteoporosis is caused by osteoclast hy-perfunction, loss of tissue integrity due to “ senescent ” fibroblast hy-perfunction (Campisi, 2013; Gems and Kern, 2022), or mTOR-promoted stem cell loss (Blagosklonny, 2008a).”
Targeting immunosenescence for improved tumor immunotherapy
Liu, Z., Zuo, L., Zhou, Z., Liu, S., Ba, Y., Zuo, A., Ren, Y., Zhang, C., Chen, Y., Ma, H., et al. (2024) · MedComm · doi:10.1002/mco2.777 · Cited by 24
“70 SASP has been confirmed to launch spontaneous DNA damage in immune cells and higher senescence and SASP markers in various immune cells, such as monocytes/macrophages, B cells, NK cells, and T cells.”
BackgroundSong, C., Liu, F., Wu, X., Zhou, D., Mei, Y., Yan, Q., Yan, Q., Liu, Z., & Chen, F. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.114131 · Cited by 26
Admasu, T. D., & Yu, J. S. (2025) · Aging Cell · doi:10.1111/acel.70055 · Cited by 30
“However, continuous proliferation increases mutation risk, driving genomic instability and senescence (Liu et al. 2023; Campisi 2013).”
Targeting CDKs in cancer therapy: advances in PROTACs and molecular glues
Marei, H. E. S., Bedair, K., Hasan, A., Al-Mansoori, L., Gaiba, A., Morrione, A., Cenciarelli, C., & Giordano, A. (2025) · npj Precision Oncology · doi:10.1038/s41698-025-00931-8 · Cited by 31
Cell and molecular response to IORT treatment
Minafra, L., & Bravatà, V. (2014) · Nova Science Publishers (Nova Science Publishers, Inc.) · doi:10.21037/2092 · Cited by 29
“These characteristics are defined as senescence associated secretory phenotype (SASP) (64-67).”
BackgroundMarmisolle, I., Martínez, J., Liu, J., Mastrogiovanni, M., Fergusson, M. M., Rovira, I. I., Castro, L., Trostchansky, A., Moreno, M., Cao, L., et al. (2016) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2016.10.016 · Cited by 23
“In addition to the lack of proliferation, senescent cells exhibit characteristic morphological changes, senescenceassociated β-galactosidase expression (SA-β-Gal) due to an increase in lysosomal content, activation of the DNA damage response (DDR), heterochromatic foci and a secretory phenotype [1, 2].”
BackgroundRapid Telomere Reduction in Cancer Cells Induced by G-Quadruplex-Targeting Copper Complexes
Yu, Z., Carter-Fenk, K., Huang, D., Sen, S., & Cowan, J. A. (2019) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.9b00215 · Cited by 24
Chromatin remodeling factor BAZ1A regulates cellular senescence in both cancer and normal cells
Li, X., Ding, D., Yao, J., Zhou, B., Shen, T., Qi, Y., Ni, T., & Wei, G. (2019) · Life Sciences · doi:10.1016/j.lfs.2019.05.023 · Cited by 26
Aging-related genes are potential prognostic biomarkers for patients with gliomas
Xiao, G., Zhang, X., Zhang, X., Chen, Y., Xia, Z., Cao, H., Huang, J. X., & Cheng, Q. (2021) · Aging · doi:10.18632/aging.203008 · Cited by 24
Smith, S., Hoelzl, F., Zahn, S., & Criscuolo, F. (2021) · Molecular Ecology · doi:10.1111/mec.16233 · Cited by 22
“For instance, cell senescence also promotes regular tissue repair, and protects against cell immortalization and cancer, while at the same time triggering pro-82 inflammatory or tissue degeneration processes (reviewed in Autexier & Lue, 2006; Campisi, 2013).”
BackgroundIntegrin β3 Induction Promotes Tubular Cell Senescence and Kidney Fibrosis
Shen, L., Jiang, S., Zhang, Q., Jin, B. R., Lv, D., Li, W., Zhao, M., Jiang, C., Dai, C., & Liu, Z. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.733831 · Cited by 27
“The passive Heymann nephritis (PHN) model was established as previously described in our lab (Chen et al., 2010).”
MethodLi, L., Chen, Y., & Shi, C. Q. (2022) · Bioengineered · doi:10.1080/21655979.2022.2036913 · Cited by 24
“Cell senescence refers to irreversible cell cycle stagnation caused by activation of a series of intracellular signaling pathways under the stimulation of a variety of internal and external factors, which are mainly characterized by chromatin changes, changes in cell metabolism and morphology, and enhanced activity of…”
BackgroundSenotherapeutics in Cancer and HIV
Sánchez-Díaz, L., Espinosa-Sánchez, A., Blanco, J. R., & Carnero, A. (2022) · Cells · doi:10.3390/cells11071222 · Cited by 27
Senotherapies: A novel strategy for synergistic anti-tumor therapy
Qi, X., Li, J., & Cao, J. (2022) · Drug Discovery Today · doi:10.1016/j.drudis.2022.103365 · Cited by 25
Emerging Role of Nicotinamide Riboside in Health and Diseases
Sharma, C., Donu, D., & Cen, Y. (2022) · Nutrients · doi:10.3390/nu14193889 · Cited by 24
“Many inflammation-related conditions—such as Alzheimer’s disease (AD), sclerosis, and fibrosis—are known to deplete NAD+ contents, aggravate cellular injury, and upregulate proinflammatory cytokines [19,61].”
BackgroundTargeting Cellular Senescence with Senotherapeutics: Development of New Approaches for Skin Care
Thompson, E. L., Pitcher, L. E., Niedernhofer, L. J., & Robbins, P. D. (2021) · Plastic & Reconstructive Surgery · doi:10.1097/prs.0000000000009668 · Cited by 26
Senescent Stromal Cells in the Tumor Microenvironment: Victims or Accomplices?
Ye, M., Huang, X., Wu, Q., & Liu, F. (2023) · Cancers · doi:10.3390/cancers15071927 · Cited by 27
“In addition, other factors that cause stromal cell senescence in the TME include nutrition dysregulation [40], age [8,61,62], microbiota dysbiosis with toxin [40,63], and so on.”
BackgroundYing, H., Li, Z., Li, M.-P., & Liu, W. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1217669 · Cited by 29
Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway
Jin, C.-W., Wang, H., Chen, Y., Tang, M., Fan, G., Wang, Z., Li, L., Zhang, Y., Zhang, W., & Zhong, M. (2015) · Cellular Physiology and Biochemistry · doi:10.1159/000373940 · Cited by 25
Male Sex is an Inherent Risk Factor for Basal Cell Carcinoma
Bassukas, I. D., & Tatsioni, A. (2019) · Journal of Skin Cancer · doi:10.1155/2019/8304271 · Cited by 24
“Age and sex are two major, nonmodiable factors of the risk of an individual to be diagnosed with cancer [3] and together these two factors signicantly modulate the incidence of the disease at the population level: Cancer is a disease of aging [4] and taking all age groups together a disease that is more frequent in…”
BackgroundMiyajima, C., Kawarada, Y., Inoue, Y., Suzuki, C., Mitamura, K., Morishita, D., Ohoka, N., Imamura, T., & Hayashi, H. (2020) · Cells · doi:10.3390/cells9010171 · Cited by 24
“The senescence program is initiated and maintained by the p53-p21 and p16 Ink4a -pRB pathways [36].”
BackgroundViel, T. A., Chinta, S. J., Rane, A., Chamoli, M., Buck, H. S., & Andersen, J. K. (2020) · Aging · doi:10.18632/aging.103449 · Cited by 25
Gene expression markers of age-related inflammation in two human cohorts
Pilling, L. C., Joehanes, R., Melzer, D., Harries, L. W., Henley, W., Dupuis, J., Lin, H., Mitchell, M., Hernandez, D., Ying, S.-X., et al. (2015) · Experimental Gerontology · doi:10.1016/j.exger.2015.05.012 · Cited by 24
“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 et al., 2013), may also be a possible cause.”
Pathogenesis of Warthin’s Tumor: Neoplastic or Non-Neoplastic?
Aoki, R., & Tanaka, T. (2024) · Cancers · doi:10.3390/cancers16050912 · Cited by 24
“Thus, cellular senescence has a dual nature: inhibiting tumors while promoting Thus, cellular senescence has a dual nature: inhibiting tumors while promoting them [57,61–63]. promoting them [57,61 – 63].”
BackgroundCen, P., Cui, C., Huang, J., Chen, H., Wu, F. H., Niu, J., Zhong, Y., Jin, C., Zhu, W., Zhang, H., et al. (2024) · Acta Biomaterialia · doi:10.1016/j.actbio.2024.03.027 · Cited by 25
Stem cell activity-coupled suppression of endogenous retrovirus governs adult tissue regeneration
Lyu, Y., Kim, S., Humphrey, E., Nayak, R., Guan, Y., Liang, Q., Kim, K. H., Tan, Y., Dou, J., Sun, H., et al. (2024) · Cell · doi:10.1016/j.cell.2024.10.007 · Cited by 31
The interplay between cell death and senescence in cancer
Shimizu, K., Inuzuka, H., & Tokunaga, F. (2024) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2024.11.001 · Cited by 28
Circadian disruption-induced microRNAome deregulation in rat mammary gland tissues
Kochan, D. Z., Ilnytskyy, Y., Golubov, A., Deibel, S. H., McDonald, R. J., & Kovalchuk, O. (2015) · Oncoscience · doi:10.18632/oncoscience.157 · Cited by 23
“Cellular senescence is a response to extracellular and intracellular stresses, such as oncogenic stimuli, that causes permanent cell-cycle arrest and acts as a potent tumour suppression mechanism that prevents the oncogenic transformation of primary cells [39].”
BackgroundLoss of the ubiquitin conjugating enzyme UBE2E3 induces cellular senescence
Plafker, K. S., Zyla, K., Berry, W. L., & Plafker, S. M. (2018) · Redox Biology · doi:10.1016/j.redox.2018.05.008 · Cited by 24
Krüppel-Like Factor 6 Is Required for Oxidative and Oncogene-Induced Cellular Senescence
Sabatino, M. E., Castellaro, A., Racca, A. C., Carbajosa González, S., Pansa, M. F., Soria, G., & Bocco, J. L. (2019) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2019.00297 · Cited by 23
“Frequently, cells with high levels of DNA damage can trigger cellular senescence and steadily lose their ability to undergo cell proliferation (Campisi, 2013).”
BackgroundThyroid hormone induces cellular senescence in prostate cancer cells through induction of DEC1
Kotolloshi, R., Mirzakhani, K., Ahlburg, J., Kraft, F., Pungsrinont, T., & Baniahmad, A. (2020) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2020.105689 · Cited by 25
Balasubramanian, P., Branen, L., Sivasubramanian, M. K., Monteiro, R., & Subramanian, M. (2021) · Aging · doi:10.18632/aging.203111 · Cited by 23
“Cellular senescence is a state of irreversible growth arrest that occurs in proliferating cells in response to cellular damage or sub-lethal stress induced by telomere shortening, oxidative stress, oncogene activation, DNA damage or mitochondrial dysfunction [13].”
BackgroundThe tumor suppression theory of aging
Wolf, A. M. (2021) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2021.111583 · Cited by 27
“Cell senescence artificially limits a cell’s capacity for self-renewal (Campisi, 2013) and the robust association of senescent cells with cancer illustrates that cellular senescence primarily works as a barrier to malignant tumorigenesis in vivo (Burd et al., 2013).”
BackgroundShen, C., Lu, C., Wu, C.-H., Li, K., Kuo, Y., Hsieh, S., & Yu, C. (2021) · Cells · doi:10.3390/cells10123402 · Cited by 22
“IL-8, macrophage inflammatory proteins (MIPs), and membrane cofactor proteins (MCPs) to elicit inflammation [100].”
BackgroundMesenchymal Stem Cell Senescence and Osteogenesis
Tjempakasari, A., Suroto, H., & Santoso, D. (2021) · Medicina · doi:10.3390/medicina58010061 · Cited by 25
Chen, M., Wen, H., Zhou, S., Yan, X., & Li, H. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/6821170 · Cited by 23
“Senescence is regarded as one of important drivers in many diseases and has been linked to articular disease such as osteoporosis, macular degeneration, and osteoarthritis (OA) [3].”
Protective roles of cytoplasmic p21Cip1 /Waf1 in senolysis and ferroptosis of lung cancer cells
Koyanagi, A., Kotani, H., Iida, Y., Tanino, R., Kartika, I. D., Kishimoto, K., & Harada, M. (2022) · Cell Proliferation · doi:10.1111/cpr.13326 · Cited by 22
“Therefore, TIS has been considered a major hurdle that must be overcome to improve the prognosis of cancer patients receiving anticancer therapies.(9,10) Received: 1 June 2022 Revised: 10 July 2022 Accepted: 1 August 2022”
BackgroundHolmberg, C., Wolf, A., Olsson, M. M., & Heckemann, B. (2022) · International Journal of Nursing Studies · doi:10.1016/j.ijnurstu.2022.104379 · Cited by 23
Sourki, P. A., Pourfathollah, A. A., Kaviani, S., Zomorrod, M. S., Ajami, M., Wollenberg, B., Multhoff, G., & Dezfouli, A. B. (2023) · Experimental Gerontology · doi:10.1016/j.exger.2023.112142 · Cited by 26
“tionality during aging due to their irreversibly cell-cycle arrest and nonproliferative state (Campisi, 2013).”
InfluentialYang, L., Chen, X., Lee, C., Shi, J., Lawrence, E. B., Zhang, L., Li, Y., Gao, N., Jung, S. Y., Creighton, C. J., et al. (2023) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-023-02689-y · Cited by 24
“Notably, such age-associated epimutations are preferentially located on CpG islands marked with polycomb complex [10] and p16, which controls cell cycle progression, promotes cellular senescence, and is one of the best documented polycomb-bound genes [11, 12].”
BackgroundDo age‐associated DNA methylation changes increase the risk of malignant transformation?
Wagner, W., Weidner, C. I., & Lin, Q. (2014) · BioEssays · doi:10.1002/bies.201400063 · Cited by 23
“Both processes involve telomere attrition, accumulation of genomic damage, oncogenes, and tumor suppressive pathways [20].”
BackgroundTesting of geroprotectors in experiments on cell cultures: Choosing the correct model system
Khokhlov, A. N., Клебанов, А. А., Karmushakov, A. F., Shilovsky, G. A., Nasonov, M. M., & Васильевна, М. Г. (2014) · Moscow University Biological Sciences Bulletin · doi:10.3103/s0096392514020035 · Cited by 23
The Heart: Mostly Postmitotic or Mostly Premitotic? Myocyte Cell Cycle, Senescence, and Quiescence
Siddiqi, S., & Sussman, M. A. (2014) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2014.08.014 · Cited by 22
Berghella, A. M., Contasta, I., Marulli, G., D’Innocenzo, C., Garofalo, F., Gizzi, F., Bartolomucci, M., Laglia, G., Valeri, M., Gizzi, M., et al. (2014) · Immunity & Ageing · doi:10.1186/1742-4933-11-3 · Cited by 23
“There is a growing consensus that the big part of chronic pathologies of ageing are linked by a common biology and that cellular senescence and the related secretion of inflammatory mediators are common factors [1,17,18].”
BackgroundReflections on the role of senescence during development and aging
Triana-Martínez, F., Pedraza-Vázquez, G., Maciel-Barón, L. Á., & Königsberg, M. (2016) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2016.04.004 · Cited by 23
Verlingue, L., Dugourd, A. J. F., Stoll, G., Barillot, E., Calzone, L., & Londoño‐Vallejo, A. (2016) · Aging Cell · doi:10.1111/acel.12504 · Cited by 25
“Persistent telomeric or genomic damages, oncogene activation, epigenomic perturbations, and/or tumor suppressor inactivation are among the main triggers of cell senescence (Campisi, 2013).”
BackgroundUnbalanced Growth, Senescence and Aging
Polymenis, M., & Kennedy, B. K. (2017) · Advances in experimental medicine and biology · doi:10.1007/978-3-319-57127-0_8 · Cited by 23
Iscador Qu inhibits doxorubicin-induced senescence of MCF7 cells
Srdić‐Rajić, T., Santibanez, J. F., Kanjer, K., Miletić, N. T., Cavic, M. R., Galun, D., Jevric, M., Kardum, N., Konić‐Ristić, A., & Zoranovic, T. (2017) · Scientific Reports · doi:10.1038/s41598-017-03898-0 · Cited by 23
Localised prostate cancer in elderly men aged 80–89 years, findings from a population‐based registry
Vatandoust, S., Kichenadasse, G., O’Callaghan, M. E., et al. (2018) · British Journal of Urology · doi:10.1111/bju.14228 · Cited by 23
Cerrito, M. G., Giorgi, M. D., Pelizzoni, D., Bonomo, S., Digiacomo, N., Scagliotti, A., Bugarin, C., Gaipa, G., Grassilli, E., Lavitrano, M., et al. (2018) · Oncotarget · doi:10.18632/oncotarget.25422 · Cited by 23
“Accordingly, it has been shown that several anticancer agents induce autophagic cell death in cell lines and animal models and finally promote tumor regression [32, 34].”
BackgroundThe Biological Basis of Radiation Oncology
Zeman, E. M. (2015) · Elsevier eBooks · doi:10.1016/b978-0-323-24098-7.00001-0 · Cited by 26
Ask, T. F., Lugo, R. G., & Sütterlin, S. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00726 · Cited by 23
“Senescent cells secrete SASP factors and cause loss of tissue structure and function (Chinta et al., 2015) which induce cancer and tumor growth and metastasis over time (Campisi, 2013; Tchkonia et al., 2013).”
BackgroundInfluentialJumonji C Demethylases in Cellular Senescence
Leon, K. E., & Aird, K. M. (2019) · Genes · doi:10.3390/genes10010033 · Cited by 22
“Therefore, senescence is considered a tumor suppression mechanism [44].”
BackgroundComparison of several commonly used detection indicators of cell senescence
Xiao, Y., Zhang, Y., & Xiao, F. (2018) · Drug and Chemical Toxicology · doi:10.1080/01480545.2018.1551407 · Cited by 23
“Cell senescence is the state of irreversible growth arrest that can be triggered by a variety of different cellular stresses including DNA damage, oncogene activation, oxidative stress, and exogenous toxicants exposure (Campisi 2013).”
BackgroundInfluentialThe Enigmatic Protein Kinase C-eta
Basu, A. (2019) · Cancers · doi:10.3390/cancers11020214 · Cited by 24
“Senescence can cause tumor suppression by inducing permanent cell cycle arrest and by recruiting immune systems to clear senescent cells [57,58].”
BackgroundHow cancer therapeutics cause accelerated aging: Insights from the hallmarks of aging
Hill, A., Sadda, J., LaBarge, M. A., & Hurria, A. (2019) · Journal of Geriatric Oncology · doi:10.1016/j.jgo.2019.03.007 · Cited by 24
Sun, X., Thorne, R. F., Zhang, X. D., He, M., Li, J., Feng, S., Liu, X., & Wu, M. (2020) · EMBO Reports · doi:10.15252/embr.201948796 · Cited by 22
“The latter function is relevant since telomere shortening or uncapping can also drive cellular senescence [21].”
Lee, Y. H., Jung, H. S., Kwon, M. J., Jang, J. E., Kim, T. N., Lee, S. H., Kim, M.-K., & Park, J. H. (2020) · Islets · doi:10.1080/19382014.2020.1783162 · Cited by 23
“As cells age, they lose cloning ability, change into a pro-inflammatory phenotype and stain positive for senescence-associated βgalactosidase activity (SA – β Gal).(22) P16 is a tumor suppressor protein and a cyclin kinase inhibitor, and increased expression is a primary driver of cellular senescence, an irreversible…”
BackgroundSenescence of human skin-derived precursors regulated by Akt-FOXO3-p27KIP1/p15INK4b signaling
Liu, S., Wang, X., Zhao, Q., Liu, S., Zhang, H., Shi, J., Li, N., Lei, X., Zhao, H., Deng, Z., et al. (2015) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-015-1877-3 · Cited by 25
TBX2 controls a proproliferative gene expression program in melanomaPreprint
Lu, S., Louphrasitthiphol, P., Goradia, N., Lambert, J., Schmidt, J., Chauhan, J. S., Rughani, M. G., Larue, L., Wilmanns, M., & Goding, C. R. (2021) · Genes & Development · doi:10.1101/gad.348746.121 · Cited by 21
“…inhibitors, chromatin reorganization, and inflammatory signaling known as the senescence-associated secretory phenotype, and can be triggered by a wide variety of cell-extrinsic and -intrinsic signals (for reviews, see Kuilman et al. 2010; Campisi 2013; He and Sharpless 2017; Herranz and Gil 2018).”
BackgroundCell enlargement modulated by GATA4 and YAP instructs the senescence-associated secretory phenotype
Joung, J., Heo, Y., Kim, Y., Kim, J., Choi, H., Jeon, T., Jang, Y., Kim, E.-J., Lee, S. H., Suh, J. M., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-56929-0 · Cited by 26
Ki, M., Kim, D. H., Abdelhamid, M. A. A., & Pack, S. P. (2025) · Biosensors · doi:10.3390/bios15110737 · Cited by 33
LY6D-induced macropinocytosis as a survival mechanism of senescent cells
Nagano, T., Iwasaki, T., Onishi, K., Awai, Y., Terachi, A., Kuwaba, S., Asano, S., Katasho, R., Nagai, K., Nakashima, A., et al. (2020) · Journal of Biological Chemistry · doi:10.1074/jbc.ra120.013500 · Cited by 21
“Cellular senescence is defined as an irreversible cell proliferation arrest induced by various stresses, such as telomere erosion, activated oncogenes, oxidative stress, and DNA damage (1, 2).”
BackgroundEvaluating the neuroprotective impact of senolytic drugs on human vision
El-Nimri, N. W., Moore, S. M., Zangwill, L. M., Proudfoot, J. A., Weinreb, R. N., Skowronska-Krawczyk, D., & Baxter, S. L. (2020) · Scientific Reports · doi:10.1038/s41598-020-78802-4 · Cited by 22
Where does cellular senescence belong in the pathophysiology of ovarian cancer?
Książek, K. (2020) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2020.11.021 · Cited by 22
Dynamic Aging: Channeled Through Microenvironment
Tan, Q., Liang, N., Zhang, X., & Li, J. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.702276 · Cited by 25
“The secretion of SASP factors change microenvironment and affect even remote tissue via paracrine, which is believed to contribute to organ degeneration with aging (Campisi, 2013).”
BackgroundMiao, X., Zhu, X., Gu, Z., Fu, B., Cui, S., Zu, Y., Rong, L.-J., Hu, F., Chen, X., Gong, Y., et al. (2022) · Cell Biochemistry and Biophysics · doi:10.1007/s12013-021-01058-w · Cited by 23
“Moreover, senescent cells are marked by sustained growth arrest that is dependent on the p53 pathway and is maintained by upregulation of p16 and p21 [31].”
BackgroundHe, S., Zhou, M., Zheng, H., Wang, Y., Wu, S., Gao, Y., & Chen, J. (2022) · Renal Failure · doi:10.1080/0886022x.2022.2029488 · Cited by 23
“Currently, as is known to all, it is induced by telomere shortening triggered signals [4].”
BackgroundMachine Learning Analysis Reveals Biomarkers for the Detection of Neurological Diseases
Lam, S. C. C., Arif, M., Song, X., Uhlén, M., & Mardinoğlu, A. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.889728 · Cited by 22
Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression
Kyi, P., Hendee, K., Hunyenyiwa, T., Matus, K., Mammoto, T., & Mammoto, A. (2022) · Frontiers in Medicine · doi:10.3389/fmed.2022.908639 · Cited by 24
“Senescent ECs play a key role in vascular aging and agerelated cardiovascular and degenerative diseases (12, 13, 15), and senolytic reagents are extensively studied in the aging research (28, 29).”
BackgroundKong, J., Sun, S., Fei, M., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232214281 · Cited by 22
“Aging is inevitable in biological organisms, and it is a multidimensional process of organismal decline [1].”
BackgroundRodríguez-Agustín, A., Casanova, V., Grau-Expósito, J., Sánchez‐Palomino, S., Alcamı́, J., & Climent, N. (2023) · Pharmaceutics · doi:10.3390/pharmaceutics15030917 · Cited by 25
Involvement of Bcl-2 Family Proteins in Tetraploidization-Related Senescence
Barriuso, D., Alvarez-Frutos, L., Gutiérrez, L. G., Motiño, O., Kroemer, G., Palacios, R., & Senovilla, L. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076374 · Cited by 23
“In turn, senescence can be induced by a variety of cellular stresses, including some chemotherapeutics, as a tumor suppressor mechanism [15].”
BackgroundProteome analysis in the assessment of ageing
Nkuipou‐Kenfack, E., Koeck, T., Mischak, H., Pich, A., Schanstra, J. P., Zürbig, P., & Schumacher, B. (2014) · Ageing Research Reviews · doi:10.1016/j.arr.2014.09.002 · Cited by 22
Possible role of ABO system in age-related diseases and longevity: a narrative review
Rizzo, C., Caruso, C., & Vasto, S. (2014) · Immunity & Ageing · doi:10.1186/1742-4933-11-16 · Cited by 22
“Clinical and epidemiological studies, in fact, show a strong association between chronic infections, inflammation and cancer and indicate that, even in tumours not directly linked to pathogens, the microenvironment is characterized by the presence of a smouldering inflammation, fuelled both by stromal leukocytes and s…”
BackgroundBadiola, I., Santaolalla, F., García-Gallastegui, P., del Rey, A. S., Unda, F. J., & Ibarretxe, G. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.03.004 · Cited by 22
Differential Matrix Metalloprotease (MMP) Expression Profiles Found in Aged Gingiva
Kim, S., Ahn, S. H., Lee, J.-S., Song, J., Cho, S.-H., Jung, S., Kim, S., Kim, S.-H., Lee, K., Kwon, K., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0158777 · Cited by 23
“Some of the biologic mechanisms that regulate aging may be involved in the pathogenesis of diseases that increase with age, such as cancer [24, 25].”
BackgroundWang, X., Dong, C., Sun, L., Zhu, L., Sun, C., Ma, R., Ning, K., Lu, B., Zhang, J., & Xu, J. (2016) · Scientific Reports · doi:10.1038/srep37443 · Cited by 23
Costarelli, L., Giacconi, R., Malavolta, M., Basso, A., Piacenza, F., Provinciali, M., Maggio, M. G., Corsonello, A., & Lattanzio, F. (2016) · Biogerontology · doi:10.1007/s10522-016-9675-3 · Cited by 22
“Conversely, a persistent SASP production can cause local and systemic inflammation, disrupt tissue architecture, and stimulate growth of nearby malignant cells (Rodier and Campisi 2011).”
InfluentialPorta, C. A. M. L., & Zapperi, S. (2017) · Cambridge University Press eBooks · doi:10.1017/9781316271759 · Cited by 24
Yang, L., Xing, S., Wang, K., Hua, Y., & Du, B. (2017) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-017-3141-7 · Cited by 23
Zhang, W., Zhang, Y., Hou, J., Xu, T., Yin, W., Xiong, W., Lu, W., Zheng, H., Chen, J., & Yuan, J. (2017) · Environmental Toxicology and Pharmacology · doi:10.1016/j.etap.2017.08.028 · Cited by 22
Pachymic acid promotes induction of autophagy related to IGF-1 signaling pathway in WI-38 cells
Lee, S.-G., & Kim, M. (2017) · Phytomedicine · doi:10.1016/j.phymed.2017.09.020 · Cited by 21
Endothelial Cell Senescence in the Pathogenesis of Endothelial Dysfunction
Carracedo, J., Ramírez-Carracedo, R., Alique, M., & Ramı́rez, R. (2018) · InTech eBooks · doi:10.5772/intechopen.73024 · Cited by 27
“Cellular senescence is an irreversible process typical for all cells in which cells leave the cycle division as a consequence of the cellular damage associated with diseases [28] and aging [29].”
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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