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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The limited in vitro lifetime of human diploid cell strains
Hayflick, L. (1965) · Experimental Cell Research · doi:10.1016/0014-4827(65)90211-9 · Cited by 5,876
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 1×
“The first report of what is now termed oncogene-induced senescence showed that an oncogenic form of H-RAS (H-RASV12), which chronically stimulates the mitogen-activated protein kinase (MAPK) signaling pathway, provokes senescence in normal cells (45).”
BackgroundThe senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
Self-citationCellular senescence: when bad things happen to good cells
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Immune Aging and Immunotherapy in Cancer
Kaiser, M., Semeraro, M. D., Herrmann, M., Absenger, G., Gerger, A., & Renner, W. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22137016 · Cited by 79
“Unlike apoptosis, another cell-cycle exit program that results in cell death, senescent cells remain viable and most of them secrete numerous proinflammatory cytokines, chemokines, growth factors, and proteases, a feature termed senescence-associated secretory phenotype (SASP), which can have deleterious effects on th…”
BackgroundAlle, Q., Le Borgne, E., Bensadoun, P., Lemey, C., Béchir, N., Gabanou, M., Estermann, F., Bertrand‐Gaday, C., Pessemesse, L., Toupet, K., et al. (2022) · Aging Cell · doi:10.1111/acel.13714 · Cited by 66
“…cell and tissue vulnerability and deterioration and increases the risk of developing diseases like cancer, cardiovascular disorders, diabetes, atherosclerosis, age- related macular degeneration or neurodegeneration and ultimately precipitating death (Campisi, 2013; López- Otín et al., 2013).”
BackgroundKim, H., Chang, J., Iyer, S., Han, L., Campisi, J., Manolagas, S. C., Zhou, D., & Almeida, M. (2019) · Aging Cell · doi:10.1111/acel.12923 · Cited by 74
“…is characterized by a permanent proliferative arrest, and an altered gene expression pattern leading to the production of pro‐inflammatory and matrix‐degrading molecules known as the senescence‐associated secretory phenotype (SASP) (Campisi, 2013; Coppe et al., 2008; Kuilman et al., 2008).”
BackgroundSelf-citationChang, Z., Xia, J., Wu, H., Peng, W., Jiang, F., Li, J., Liang, C., Zhao, H., Park, K., Song, G., et al. (2019) · Aging Cell · doi:10.1111/acel.12990 · Cited by 74
“Paraquat is a ROS generator that causes oxidative stress, which has been demonstrated to induce cellular senescence in replicationcompetent cell types (Campisi, 2013).”
BackgroundPiovani, D., Danese, S., Peyrin‐Biroulet, L., Nikolopoulos, G. K., & Bonovas, S. (2020) · Alimentary Pharmacology & Therapeutics · doi:10.1111/apt.15692 · Cited by 74
Targeting senescent cells improves functional recovery after spinal cord injury
Paramos-de-Carvalho, D., Martins, I., Cristóvão, A. M., Dias, A. F., Neves-Silva, D., Pereira, T., Chapela, D., Farinho, A., Jacinto, A., & Saúde, L. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109334 · Cited by 74
Association of dietary inflammatory potential, dietary oxidative balance score and biological aging
Wang, X., Sarker, S., Cheng, L., Dang, K., Hu, J., Pan, S., Zhang, J., Xu, X., & Li, Y. (2023) · Clinical Nutrition · doi:10.1016/j.clnu.2023.11.007 · Cited by 82
The role of the dynamic epigenetic landscape in senescence: orchestrating SASP expression
Dasgupta, N., Arnold, R., Equey, A., Gandhi, A., & Adams, P. D. (2024) · npj Aging · doi:10.1038/s41514-024-00172-2 · Cited by 93
“This secretome comprises various proin fl ammatory cytokines, chemokines, growth factors, and proteases, collectively known as the senescence-associated secretory phenotype (SASP) 7,8 .”
BackgroundVitamin C alleviates aging defects in a stem cell model for Werner syndrome
Li, Y., Zhang, W., Chang, L., Han, Y., Sun, L., Gong, X., Tang, H., Liu, Z., Deng, H., Ye, Y., et al. (2016) · Protein & Cell · doi:10.1007/s13238-016-0278-1 · Cited by 79
“…is defined as a time-dependent deterioration of organism’s physiological functions that leads to loss of homeostasis and consequently increases susceptibility to morbidity and mortality (Benayoun et al., 2015; Burtner and Kennedy, 2010; Campisi, 2013; Kudlow et al., 2007; LopezOtin et al., 2013).”
BackgroundBone as a Preferential Site for Metastasis
Sowder, M. E., & Johnson, R. W. (2018) · JBMR Plus · doi:10.1002/jbm4.10126 · Cited by 75
“With increasing age, more cells enter an irreversible senescent state, which is associated with a senescence-associated secretory phenotype (SASP).((112)) This SASP results in the elevated secretion of cytokines, chemokines, and growth factors that may establish a tumor-promoting microenvironment that can act on surro…”
BackgroundBeauvarlet, J., Bensadoun, P., Darbo, E., Labrunie, G., Rousseau, B., Richard, E., Draskovic, I., Londono-Vallejo, A., Dupuy, J.-W., Nath Das, R., et al. (2019) · Nucleic Acids Research · doi:10.1093/nar/gkz095 · Cited by 73
Kim, Y. Y., Um, J., Yoon, J.-H., Lee, D., Lee, Y. J., Kim, D. H., Park, J., & Yun, J. (2019) · The FASEB Journal · doi:10.1096/fj.201901747rr · Cited by 74
Phenotypic and functional characterization of corneal endothelial cells during in vitro expansion
Frausto, R. F., Swamy, V. S., Peh, G. S. L., Boere, P. M., Hanser, E. M., Chung, D. D., George, B. L., Morselli, M., Kao, L., Azimov, R., et al. (2020) · Scientific Reports · doi:10.1038/s41598-020-64311-x · Cited by 73
“While senescence is generally an irreversible cell state (Campisi, 2013), CEnC from younger donors are characterized by a quiescent cell state (G1 cell cycle arrest), which is a reversible mitotic arrest that enables these cells to undergo mitogen-induced cell cycle re-entry (Joyce, 2005).”
BackgroundVelichko, A. K., Petrova, N. V., Razin, S. V., & Kantidze, O. L. (2015) · Nucleic Acids Research · doi:10.1093/nar/gkv573 · Cited by 74
Cavinato, M. S., Kozieł, R., Romani, N., Weinmüllner, R., Jenewein, B., Hermann, M., Dubrac, S., Ratzinger, G., Grillari, J., Schmuth, M., et al. (2016) · The Journals of Gerontology Series A · doi:10.1093/gerona/glw150 · Cited by 82
Bull, C. F., Mayrhofer, G., O’Callaghan, N. J., Au, A. Y. M., Pickett, H. A., Low, G. K. M., Zeegers, D., Hande, M. P., & Fenech, M. F. (2013) · Cancer Prevention Research · doi:10.1158/1940-6207.capr-13-0264 · Cited by 72
“Furthermore, senescence-induced inflammation has been associated with enhanced cancer promotion (44), an effect likely to be increased when telomeres are damaged”
BackgroundCaveolin-1, a master regulator of cellular senescence
Volonté, D., & Galbiati, F. (2020) · Cancer and Metastasis Reviews · doi:10.1007/s10555-020-09875-w · Cited by 79
Modulation of the Senescence-Associated Inflammatory Phenotype in Human Fibroblasts by Olive Phenols
Menicacci, B., Cipriani, C., Margheri, F., Mocali, A., & Giovannelli, L. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18112275 · Cited by 75
“Cellular senescence is characterized by complex modifications in the protein expression profile of the cell, leading to replicative arrest and cell dysfunction [1].”
BackgroundThe interplay between immunity and aging in Drosophila
Garschall, K., & Flatt, T. (2018) · F1000Research · doi:10.12688/f1000research.13117.1 · Cited by 69
Therapeutic Potential of Senolytics in Cardiovascular Disease
Dookun, E., Passos, J. F., Arthur, H. M., & Richardson, G. D. (2022) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-020-07075-w · Cited by 69
SirT3 and p53 Deacetylation in Aging and Cancer
Chen, J., Wang, A., & Chen, Q. (2017) · Journal of Cellular Physiology · doi:10.1002/jcp.25669 · Cited by 73
“SASP factors also induce phenotypes that are associated with progressive carcinogenesis (Campisi et al., 2011; Campisi, 2013). p53 and p53 Deacetylation p53 was first discovered as a protein that formed a complex with the SV40 tumor-virus oncoprotein, the large T-antigen, which was required for…”
BackgroundAPE1 deficiency promotes cellular senescence and premature aging features
Li, M., Yang, X., Lu, X., Dai, N., Zhang, S., Cheng, Y., Zhang, L., Yang, Y., Liu, Y., Yang, Z., et al. (2018) · Nucleic Acids Research · doi:10.1093/nar/gky326 · Cited by 72
Aging Fits the Disease Criteria of the International Classification of Diseases
Khaltourina, D. A., Matveyev, Y., Alekseev, A., Cortese, F., & Ioviţă, A. (2020) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2020.111230 · Cited by 78
Cellular Senescence: Mechanisms, Morphology, and Mouse Models
Beck, J. A., Horikawa, I., & Harris, C. C. (2020) · Veterinary Pathology · doi:10.1177/0300985820943841 · Cited by 80
“Secreted SASP chemokines recruit inflammatory cells, such as macrophages, which help remove senescent cells and restore normal tissue functions.(21,49,100,101) However, in some cases, senescent cells are not effectively removed.”
BackgroundSenescence and Apoptosis During in vitro Embryo Development in a Bovine Model
Ramos‐Ibeas, P., Gimeno, I., Cañón-Beltrán, K., Gutiérrez‐Adán, A., Rizos, D. V., & Gómez, E. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.619902 · Cited by 74
“Although cellular senescence has been mainly associated with tumor suppression, tissue repair or aging (Baker et al., 2011; Campisi, 2013; Ritschka et al., 2017), features of senescence have been also reported in cells from different mammalian species during embryonic development (Rhinn et al.,…”
BackgroundGrowth Differentiation Factor-15 in Immunity and Aging
Pence, B. D. (2022) · Frontiers in Aging · doi:10.3389/fragi.2022.837575 · Cited by 68
p53 directs leader cell behavior, migration, and clearance during epithelial repair
Kozyrska, K., Pilia, G., Vishwakarma, M., Wagstaff, L., Goschorska, M., Cirillo, S., Mohamad, S., Gallacher, K., Salas, R. E. C., & Piddini, E. (2022) · Science · doi:10.1126/science.abl8876 · Cited by 80
“While imaging colonies of wild-type MDCK cells, we observed the emergence of cells with a flattened morphology, resembling senescent cells (16) (Fig.”
BackgroundMitochondrial fatty acid oxidation drives senescence
Yamauchi, S., Sugiura, Y., Yamaguchi, J., Zhou, X., Takenaka, S., Odawara, T., Fukaya, S., Fujisawa, T., Naguro, I., Uchiyama, Y., et al. (2024) · Science Advances · doi:10.1126/sciadv.ado5887 · Cited by 74
Inflammation: a matter of immune cell life and death
Bender, E. C., Tareq, H. S., & Suggs, L. J. (2025) · npj Biomedical Innovations. · doi:10.1038/s44385-025-00010-4 · Cited by 80
The intrinsic stiffness of human trabecular meshwork cells increases with senescence
Morgan, J. T., Raghunathan, V. K., Chang, Y.-R., Murphy, C. J., & Russell, P. (2015) · Oncotarget · doi:10.18632/oncotarget.3798 · Cited by 71
“Further, as glaucoma has many of the hallmarks of AADs, there is substantial potential that these findings may provide insight into other AADs.”
BackgroundInfluentialGolomb, L., Sagiv, A., Pateras, I. S., Maly, A., Krizhanovsky, V, Gorgoulis, V. G., Oren, M., & Ben-Yehuda, A. (2015) · Cell Death & Differentiation · doi:10.1038/cdd.2015.21 · Cited by 71
“Yet, aging remains the strongest single risk factor for cancer development.(1,2) One example of an age-related cancer is cutaneous squamous cell carcinoma (SCC).”
BackgroundKumar, V., Pandey, A., Jahan, S., Shukla, R. K., Kumar, D., Srivastava, A., Singh, S., Rajpurohit, C. S., Yadav, S., Khanna, V. K., et al. (2016) · Scientific Reports · doi:10.1038/srep28142 · Cited by 71
Wood, W. A., Krishnamurthy, J., Mitin, N., Torrice, C., Parker, J. S., Snavely, A. C., Shea, T. C., Serody, J. S., & Sharpless, N. E. (2016) · EBioMedicine · doi:10.1016/j.ebiom.2016.08.029 · Cited by 73
“…by activation of tumor suppressor mechanisms associated with cellular stressors, and results in expression of the p16INK4a tumor suppressor protein encoded by the CDKN2a locus, which has emerged as one of the more useful markers of senescence in vivo (Campisi, 2013; Sharpless and Sherr, 2015).”
BackgroundCherry, C., Andorko, J. I., Krishnan, K., Mejías, J. C., Nguyen, H. H., Stivers, K. B., Gray-Gaillard, E. F., Ruta, A., Han, J., Hamada, N., et al. (2023) · GeroScience · doi:10.1007/s11357-023-00785-7 · Cited by 66
“Senescent cells (SnCs) are actively implicated in multiple age-related pathologies including heart disease, diabetes, neurodegeneration, cancer, and fibrosis [1–7].”
BackgroundThe Link Between Epigenetic Clocks for Aging and Senescence
Wagner, W. (2019) · Frontiers in Genetics · doi:10.3389/fgene.2019.00303 · Cited by 71
“, 2013), but it remains to be proven if the underlying mechanisms for senescence and aging are directly related (Campisi, 2013).”
BackgroundMetformin effects on head and neck squamous carcinoma microenvironment: Window of opportunity trial
Curry, J., Johnson, J. M., Tassone, P. T., Domingo‐Vidal, M., Menezes, D. W., Sprandio, J. D., Mollaee, M., Cotzia, P., Birbe, R., Lin, Z., et al. (2017) · The Laryngoscope · doi:10.1002/lary.26489 · Cited by 72
Yanagi, S., Tsubouchi, H., Miura, A., Matsuo, A., Matsumoto, N., & Nakazato, M. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18030503 · Cited by 74
Wu, Q., Allouch, A., Martins, I., Brenner, C., Modjtahedi, N., Deutsch, É., & Perfettini, J. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00613 · Cited by 76
“Persistent DNA damage activates p53 that induces p21 expression and cell cycle arrest (24).”
BackgroundInfluentialSTAT3 Regulates the Onset of Oxidant-induced Senescence in Lung Fibroblasts
Waters, D. W., Blokland, K. E. C., Pathinayake, P. S., Wei, L., Schuliga, M. J., Jaffar, J., Westall, G. P., Hansbro, P. M., Prêle, C. M., Mutsaers, S. E., et al. (2019) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2018-0328oc · Cited by 75
Misawa, T., Tanaka, Y., Okada, R., & Takahashi, A. (2020) · Geriatrics and gerontology international/Geriatrics & gerontology international · doi:10.1111/ggi.13928 · Cited by 73
Cao, Y., Yao, M., Wu, Y., Ma, N., Liu, H., & Zhang, B. (2020) · Translational Oncology · doi:10.1016/j.tranon.2020.100783 · Cited by 67
Micronuclei, inflammation and auto-immune disease
Kirsch‐Volders, M., Bolognesi, C., Ceppi, M., Bruzzone, M., & Fenech, M. F. (2020) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2020.108335 · Cited by 71
Kim, H.-J., Kim, W. J., Shin, H., Yoon, H., Moon, J.-I., Lee, E., Lim, J., Cho, Y., Lee, M., Kim, H., et al. (2022) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-022-04186-5 · Cited by 69
“Inflammatory and immune-modulatory cytokines and chemokines secreted by senescent cells can extend cellular senescence and alter the microenvironment to the direction favorable for senescence [25].”
BackgroundMitochondrial maintenance failure in aging and role of sexual dimorphism
Tower, J. (2014) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2014.10.008 · Cited by 68
Induction of dormancy in hypoxic human papillomavirus-positive cancer cells
Hoppe‐Seyler, K., Bossler, F., Lohrey, C., Bulkescher, J., Rösl, F., Jansen, L., Mayer, A., Vaupel, P. W., Dürst, M., & Hoppe‐Seyler, F. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1615758114 · Cited by 72
“The evasion from senescence by hypoxic HPV-positive cancer cells could be crucial for the pathogenesis of HPV-positive cancers, in that it allows escape from a major tumor-suppressive defense mechanism of the cell (7).”
BackgroundInfluentialMalavolta, M., Pierpaoli, E., Giacconi, R., Costarelli, L., Piacenza, F., Basso, A., Cardelli, M., & Provinciali, M. (2016) · Current Drug Targets · doi:10.2174/1389450116666150907105104 · Cited by 68
Wang, X., Lu, W., Xia, X., Zhu, Y., Ge, C., Guo, X., Zhang, N., Chen, H., & Xu, S. (2022) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2022.114266 · Cited by 70
Kilic Eren, M., Kilincli, A., & Eren, Ö. (2015) · PLOS ONE · doi:10.1371/journal.pone.0124837 · Cited by 68
“Replicative senescence was first described by Hayflick and Moorhead in 1961 in normal mammalian cells characterized by a finite replicative potential, limiting their lifespan to a certain number of divisions [19], currently known to be induced via signals triggered by telomere shortening [20].”
BackgroundTelomeric aging: mitotic clock or stress indicator?
Koliada, A. K., Krasnienkov, D. S., & Vaiserman, A. M. (2015) · Frontiers in Genetics · doi:10.3389/fgene.2015.00082 · Cited by 67
“…with damaged DNA and protection against cancerogenesis (through the activation mechanisms of cell cycle arrest or double-strand breaks-induced apoptosis), but it may also impair the cell function contributing to degenerative organ failure and organismal aging (Chen et al., 2007; Campisi, 2013).”
BackgroundA stress-induced cellular aging model with postnatal neural stem cells
Cm, D., Xl, W., Gm, W., Wj, Z., Zhu, L., Gao, S., Dj, Y., Qin, Y., Qj, L., Yl, C., et al. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.82 · Cited by 73
“Increased DNA damage and ROS are capable of activating p38 MAPK pathway that in turn can upregulate senescence genes such as p16.(4)”
BackgroundLamin in inflammation and aging
Tran, J. R., Chen, H., Zheng, X., & Zheng, Y. (2016) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2016.03.004 · Cited by 66
CCN2 induces cellular senescence in fibroblasts
Jun, J.-I., & Lau, L. F. (2016) · Journal of Cell Communication and Signaling · doi:10.1007/s12079-016-0359-1 · Cited by 66
The emerging role of ECM crosslinking in T cell mobility as a hallmark of immunosenescence in humans
Moreau, J.-F., Pradeu, T., Grignolio, A., Nardini, C., Castiglione, F., Tieri, P., Capri, M., Salvioli, S., Taupin, J.-L., Garagnani, P., et al. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2016.11.005 · Cited by 67
Flavonoids: Broad Spectrum Agents on Chronic Inflammation
Lim, H. A., Heo, M. Y., & Kim, H. P. (2019) · Biomolecules & Therapeutics · doi:10.4062/biomolther.2019.034 · Cited by 72
Cellular senescence is a promising target for chronic wounds: a comprehensive review
Wang, Z., & Shi, C. (2020) · Burns & Trauma · doi:10.1093/burnst/tkaa021 · Cited by 73
“These molecules can change the microenvironment and play an important role in a wide range of biological processes from physiology to pathology [33, 34].”
BackgroundGeroconversion of aged muscle stem cells under regenerative pressure
Sousa-Victor, P., Perdiguero, E., & Muñoz-Cánoves, P. (2014) · Cell Cycle · doi:10.4161/15384101.2014.965072 · Cited by 68
Emerging functions of circular RNA in aging
Kim, E., Kim, Y. K., & Lee, S. (2021) · Trends in Genetics · doi:10.1016/j.tig.2021.04.014 · Cited by 69
Kovács, Z., Brunner, B., & Ari, C. (2021) · Nutrients · doi:10.3390/nu13072197 · Cited by 68
Wang, F., Li, Z., Chen, L., Yang, T., Liang, B., Zhang, Z., Shao, J., Xu, X., Yin, G., Wang, S., et al. (2022) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2022.03.014 · Cited by 72
Aging of Liver in Its Different Diseases
Radonjić, T., Dukić, M., Jovanović, I., Zdravkovic, M. D., Mandić, O., Popadić, V., Popović, M., Nikolić, N., Klašnja, S., Divac, A., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232113085 · Cited by 77
“The metabolism of senescent cells is distinct from non-senescent cells and they are metabolically active regardless of the cell cycle arrest [7].”
BackgroundStress granules counteract senescence by sequestration of PAI‐1
Omer, A., Patel, D. M., Lian, X. J., Sadek, J., Marco, S. D., Pause, A., Gorospe, M., & Gallouzi, I. (2018) · EMBO Reports · doi:10.15252/embr.201744722 · Cited by 69
“…growth hormones, cytokines, angiogenic factors, and extracellular matrix-remodeling proteases (e.g. GROa1, IL-6, IL-8, and PAI-1) that affect tissues locally and systemically, thereby accelerating or suppressing cancer development or other age-associated conditions like atherosclerosis [1,7,17,18].”
InfluentialModeling Late-Onset Sporadic Alzheimer’s Disease through BMI1 Deficiency
Flamier, A., El Hajjar, J., Adjaye, J., Fernandes, K. J., Abdouh, M., & Bernier, G. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.04.097 · Cited by 65
Immunohistochemical Expression of p16 in Melanocytic Lesions: An Updated Review and Meta-analysis
Koh, S. S., & Cassarino, D. S. (2018) · Archives of Pathology & Laboratory Medicine · doi:10.5858/arpa.2017-0435-ra · Cited by 68
Topoisomerase 1 cleavage complex enables pattern recognition and inflammation during senescence
Zhao, B., Liu, P., Fukumoto, T., Nacarelli, T., Fatkhutdinov, N., Wu, S., Lin, J., Aird, K. M., Tang, H., Liu, Q., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-14652-y · Cited by 71
Kiss, T., Nyúl-Tóth, Á., DelFavero, J., Balasubramanian, P., Tarantini, S., Faakye, J., Gulej, R., Ahire, C., Ungvari, A., Yabluchanskiy, A., et al. (2022) · GeroScience · doi:10.1007/s11357-022-00521-7 · Cited by 66
Ghosh, D., Peña, C. M., Quach, N. D., Xuan, B., Lee, A. H., & Dawson, M. (2020) · Journal of Cell Science · doi:10.1242/jcs.232470 · Cited by 70
“The detrimental effects of accumulating senescent cells on tissues have long been recognized (Campisi, 2013); this contributes to biological aging, tissue degeneration and cancer (Muñoz-Espín and Serrano, 2014).”
BackgroundAlessio, N., Acar, M. B., Demirsoy, İ. H., Squillaro, T., Siniscalco, D., Bernardo, G. D., Peluso, G., Özcan, S., & Galderisi, U. (2020) · Aging · doi:10.18632/aging.103606 · Cited by 68
“arrest cancer growth by blocking the proliferation of transformed cells, but it can also contribute to organismal aging [1, 2].”
Lemoine, M. (2020) · Biology & Philosophy · doi:10.1007/s10539-020-09765-z · Cited by 80
“Others claim that cell senescence is the major cause of functional decline (e.g. Campisi 2013).”
BackgroundInfluentialZhang, R., Chen, H., & Liu, D. (2015) · Cell Systems · doi:10.1016/j.cels.2015.09.002 · Cited by 70
Role of thyroid hormones in the neoplastic process: an overview
Goemann, I. M., Romitti, M., Meyer, E. L. D. S., Wajner, S. M., & Maia, A. L. (2017) · Endocrine Related Cancer · doi:10.1530/erc-17-0192 · Cited by 67
“Cells can be induced to senesce via DNA damage due to increased ROS levels (Campisi 2013).”
BackgroundWhat is the role of mitochondrial dysfunction in skin photoaging?
Naidoo, K., Hanna, R., & Birch‐Machin, M. A. (2017) · Experimental Dermatology · doi:10.1111/exd.13476 · Cited by 69
“Senescent cells have been shown to accumulate with increasing age and are implicated in the pathogenesis of age-related diseases [24].”
BackgroundKim, D. E., Dollé, M. E. T., Vermeij, W. P., Gyenis, Á., Vogel, K., Hoeijmakers, J. H. J., Wiley, C. D., Davalos, A. R., Hasty, P., Desprez, P., et al. (2019) · Aging Cell · doi:10.1111/acel.13072 · Cited by 66
“Senescent cells accumulate during aging and at sites of many age-related pathologies (Campisi, 2013; Coppe, Desprez, Krtolica, & Campisi, 2010).”
BackgroundMethodInfluentialSelf-citationRhoifolin ameliorates osteoarthritis via the Nrf2/NF-κB axis: in vitro and in vivo experiments.
Chen, H., Qin, J., Shi, H.-S., Li, Q., Zhou, S.-Q., & Chen, L.-B. (2022) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2022.01.009 · Cited by 66
Picca, A., Calvani, R., Coelho‐Júnior, H. J., Marini, F., Landi, F., & Marzetti, E. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232214006 · Cited by 65
“The accumulation of senescent cells is proposed as a major mechanism driving the aging process and favoring the development of chronic degenerative diseases [15].”
BackgroundThe role of telomeres and vitamin D in cellular aging and age-related diseases
Pusceddu, I., Farrell, C.-J. L., Pierro, A. M. D., Jani, E., Herrmann, W., & Herrmann, M. (2015) · Clinical Chemistry and Laboratory Medicine (CCLM) · doi:10.1515/cclm-2014-1184 · Cited by 68
“The state of senescence is established and maintained by at least two major tumor suppressor pathways: the p53/ p21 and the p16INK4a/pRB pathways [8].”
BackgroundInfluentialHyperbilirubinemia Protects against Aging‐Associated Inflammation and Metabolic Deterioration
Zelenka, J., Dvořák, A., Alán, L., Zadinová, M., Haluzı́k, M., & Vı́tek, L. (2016) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/6190609 · Cited by 65
Giuliani, A., Prattichizzo, F., Micolucci, L., Ceriello, A., Procopio, A. D., & Rippo, M. R. (2017) · Mediators of Inflammation · doi:10.1155/2017/2309034 · Cited by 66
“Increased levels of SASP-related compounds have been reported in a number of human ARDs such as diabetes [27–29], atherosclerosis [30], and cancer [31].”
BackgroundA parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans
Wang, H., Zhao, Y., Ezcurra, M., Benedetto, A., Gilliat, A. F., Hellberg, J. E. E. U., Ren, Z., Galimov, E. R., Athigapanich, T., Girstmair, J., et al. (2018) · npj Aging and Mechanisms of Disease · doi:10.1038/s41514-018-0025-3 · Cited by 62
“However, the age-increase in cancer rate is to some degree the result of the effect on aging on the cellular microenvironment.(15) Moreover, some forms of cancer can originate with run-on rather than mutation, for example benign prostatic hyperplasia (BPH) in humans, which typically precedes prostate cancer, is the re…”
BackgroundCell Senescence, Multiple Organelle Dysfunction and Atherosclerosis
Machado-Oliveira, G., Ramos, C., Marques, A. R. A., & Vieira, O. V. (2020) · Cells · doi:10.3390/cells9102146 · Cited by 70
“In this instance, EC senescence has been proposed as a pathophysiological contributor to developing vascular disease [27].”
BackgroundSenescence: A DNA damage response and its role in aging and Neurodegenerative Diseases
Shreeya, T., Ansari, M. S., Kumar, P., Saifi, M., Shati, A. A., Alfaifi, M. Y., & Elbehairi, S. E. I. (2024) · Frontiers in Aging · doi:10.3389/fragi.2023.1292053 · Cited by 72
“Senescence can be termed as a double-edged sword: as it acts as a defense mechanism against cancer, its accumulation is associated with aging and age-related diseases (Campisi, 2013).”
BackgroundDiametrical diseases reflect evolutionary-genetic tradeoffs
Crespi, B. J., & Go, M. C. (2015) · Evolution Medicine and Public Health · doi:10.1093/emph/eov021 · Cited by 67
Natural killer cell recognition of in vivo drug-induced senescent multiple myeloma cells
Antonangeli, F., Soriani, A., Ricci, B., Ponzetta, A., Benigni, G., Morrone, S., Bernardini, G., & Santoni, A. (2016) · OncoImmunology · doi:10.1080/2162402x.2016.1218105 · Cited by 67
In the Wnt-er of life: Wnt signalling in melanoma and ageing
Kaur, A., Webster, M. R., & Weeraratna, A. T. (2016) · British Journal of Cancer · doi:10.1038/bjc.2016.332 · Cited by 64
“For example, it has long been proposed that the ageing stroma contributes to cancer progression, based on the studies using senescence as an artificial model of ageing (Campisi, 2013; Campisi and Robert, 2014).”
BackgroundRas signaling in aging and metabolic regulation
Slack, C. (2017) · Nutrition and Healthy Aging · doi:10.3233/nha-160021 · Cited by 63
“Several factors act as triggers to induce cells to senesce including telomere shortening, DNA damage and activation of oncogenic pathways including activation of Ras and chronic stimulation of MAPK signal transduction [87].”
BackgroundWogonin induces cellular senescence in breast cancer via suppressing TXNRD2 expression
Yang, D., Guo, Q., Liang, Y., Zhao, Y., Tian, X., Ye, Y., Tian, J., Wu, T., & Lu, N. (2020) · Archives of Toxicology · doi:10.1007/s00204-020-02842-y · Cited by 63
“As exit of cell cycle is a feature of senescent cells (Campisi 2013), we speculated that wogonin induced cellular senescence in these breast cancer cells.”
BackgroundAlessio, N., Aprile, D., Squillaro, T., Bernardo, G. D., Finicelli, M., Melone, M. A. B., Peluso, G., & Galderisi, U. (2019) · Aging · doi:10.18632/aging.102172 · Cited by 67
“At odds with this statement, there are many findings showing that, in some experimental conditions, senescent cells may promote cancer growth or at least be ineffective in arresting tumor cell proliferation [12, 20].”
BackgroundChae, J., Jang, H., Son, C., Park, C., Choi, H., Jin, S., Lee, H., Lee, H., Ryu, J., Kim, N., et al. (2021) · GeroScience · doi:10.1007/s11357-021-00457-4 · Cited by 64
Wang, H., Yuan, S., Zheng, Q., Zhang, S., Zhang, Q., Ji, S., Wang, W. J., Cao, Y., Guo, Y., Yang, X., et al. (2024) · Gastroenterology · doi:10.1053/j.gastro.2024.01.025 · Cited by 67
Shima, P. D., Eberhard, S., Boitard, L., Rodriguez, J. G., Wang, Y., Brémond, N., Baudry, J., Bibette, J., & Wollman, F.-A. (2015) · PLoS ONE · doi:10.1371/journal.pone.0118987 · Cited by 63
“Many studies document telomere shortening, as a contributing cause to aging and senescence in eukaryotic cells [24,107–118].”
BackgroundBAF180 regulates cellular senescence and hematopoietic stem cell homeostasis through p21
Lee, H., Dai, F., Zhuang, L., Xiao, Z., Kim, J., Zhang, Y., Ma, L., You, M. J., Wang, Z., & Gan, B. (2016) · Oncotarget · doi:10.18632/oncotarget.8102 · Cited by 65
“Senescence can be regulated by multiple pathways, most notably the p53/p21 and p16/ Rb pathways [24, 25].”
Epigenetic Basis of Cellular Senescence and Its Implications in Aging
Nacarelli, T., Liu, P., & Zhang, R. (2017) · Genes · doi:10.3390/genes8120343 · Cited by 66
Investigation of quercetin and hyperoside as senolytics in adult human endothelial cells
Hwang, H. V., Tran, D., Rebuffatti, M., Li, C., & Knowlton, A. A. (2018) · PLoS ONE · doi:10.1371/journal.pone.0190374 · Cited by 66
“The in vivo development of cellular senescence, where cells halt normal function, irreversibly cease dividing, and secrete damaging inflammatory factors, has been proposed to be one of the major drivers of aging [15].”
BackgroundGao, B., Lin, X., Jing, H., Fan, J., Ji, C., Jie, Q., Zheng, C., Wang, D., Xu, X., Hu, Y., et al. (2018) · Aging Cell · doi:10.1111/acel.12741 · Cited by 63
“It is reported that senescent cells (SnCs) accumulate in bone marrow with aging (Farr et al., 2017) and contribute to age-related pathologies through their secretion of factors contributing to the senescence-associated secretory phenotype (SASP) (Campisi, 2000, 2013; Nelson et al., 2012).”
BackgroundDiscrete Changes in Glucose Metabolism Define Aging
Ravera, S., Podestà, M., Sabatini, F., Dagnino, M., Cilloni, D., Fiorini, S., Barla, A., & Frassoni, F. (2019) · Scientific Reports · doi:10.1038/s41598-019-46749-w · Cited by 63
Mas‐Bargues, C., Sanz‐Ros, J., Román-Domínguez, A., Gimeno-Mallench, L., Inglés, M., Viña, J., & Borrás, C. (2020) · Biomolecules · doi:10.3390/biom10060957 · Cited by 64
“Cellular senescence is the consequence of several stresses by which cells lose their ability to proliferate [1].”
BackgroundPLGA nanoparticles as a platform for vitamin D-based cancer therapy
Ramalho, M. J., Loureiro, J. A., Gomes, B., Frasco, M. F., Coelho, M. A. N., & Pereira, M. D. C. (2015) · Beilstein Journal of Nanotechnology · doi:10.3762/bjnano.6.135 · Cited by 62
Oral primary care: an analysis of its impact on the incidence and mortality rates of oral cancer
Rocha, T. A. H., Thomaz, É. B. A. F., da Silva, N. C., Queiroz, R. C. D. S., de Souza, M. R., Barbosa, A. C. Q., Thumé, E., Rocha, J. V., Alvares, V., de Almeida, D. G., et al. (2017) · BMC Cancer · doi:10.1186/s12885-017-3700-z · Cited by 63
“The various stressors trigger cellular senescence, generating certain intracellular signals that modulate a distinct set of senescence-inducing signaling pathways leading to cancer [49, 50].”
BackgroundLi, X., Matsumoto, T., Takuwa, M., Ali, M. S. E. S., Hirabashi, T., Kondo, H., & Fujino, H. (2020) · Biomedicines · doi:10.3390/biomedicines8020018 · Cited by 62
RetractedTomari, H., Kawamura, T., Asanoma, K., Egashira, K., Kawamura, K., 本庄, 考., Nagata, Y., & Kato, K. (2020) · Biology of Reproduction · doi:10.1093/biolre/ioaa044 · Cited by 61
“This phenomenon has been termed the SASP or, alternatively, the senescence messaging secretome (SMS) [27, 28].”
Serine and Metabolism Regulation: A Novel Mechanism in Antitumor Immunity and Senescence
Wu, Q., Chen, X., Li, J., & Sun, S. (2020) · Aging and Disease · doi:10.14336/ad.2020.0314 · Cited by 65
“hostile tissue environments; and to evade attack by the immune system, which are the hallmarks of cancer [94].”
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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