The DOI matches its Crossref record; 120 of the 122 references it cites were found in a registry or an index; none of the 43 sources its claims cite is checked for support yet.
Stress, cell senescence and organismal ageing
Open accessAbstract
Cellular senescence was first described by Hayflick and Moorhead in the 1960s as the irreversible arrest of cells following prolonged cultivation. Telomere shortening is the key mechanism driving replicative senescence in human fibroblasts. Later, pioneering work by Olivier Toussaint and others showed that stress plays a major role in the induction of senescence in vitro, a phenomenon known as stress-induced premature senescence or SIPS. It is also now widely accepted that senescence plays a role in vivo. An emerging body of evidence from animal models, and particularly mice, has demonstrated an important role for senescence in several processes such as embryonic development, wound healing, tumour suppression and ageing. However, mostly due to a lack of availability of tissues and specific markers, less is known about the importance of cell senescence in humans. In this review, we summarize some of the key findings in the field of senescence, stress-induced senescence and telomeres. We focus particularly on the role of telomere dysfunction and senescence during the ageing process as well as potential interventions, including pharmacological approaches like telomerase activators and senolytics, to counteract their detrimental effects in ageing and disease.
Overview
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Written from the paper’s full text.
TL;DR
This review summarizes cellular senescence, stress-induced premature senescence (SIPS), and telomere dysfunction, arguing that senescence may contribute to organismal ageing while human evidence remains limited. It discusses senolytics and SASP-suppressing drugs as potential interventions and highlights unresolved questions about causality and senescent-cell burden in human tissues.
Key findings
- Replicative senescence in human fibroblasts is primarily driven by telomere shortening, and ectopic telomerase expression bypasses the senescence-induced arrest. SIPS can be induced by sublethal stress in 3–10 days with no or modest telomere shortening, but persistent telomeric DNA damage can occur independently of telomere length and telomerase, so some SIPS is telomere-dependent.
- In vivo, telomere shortening occurs in some tissues and shows weak correlations with donor age; comparative data across over 60 mammalian species indicate that smaller, short-lived species tend to have long telomeres and high telomerase, and telomere length is not a limiting factor for lifespan. A human study of over 4000 people over 10 years found no association between telomere length changes and mortality or morbidity.
- Senescent cells can be beneficial (tumour suppression, wound healing, embryonic development, insulin secretion) or detrimental via the SASP. Genetic clearance of senescent cells in mice delays age-related disorders, protects from cancer, and extends median but not maximum lifespan; senolytics such as dasatinib plus quercetin, ABT-263/ABT-737, and a FOXO4 peptide improve healthspan in mouse models.
- A major challenge is the absence of a universal senescence marker; SA-β-gal has false positives, and the exact frequency of senescent cells in older tissues and healthy humans remains unknown.
Methods
- Narrative review; no primary experiments or new data are reported.
- Synthesizes published literature on cellular senescence, telomeres, SIPS, in vivo mouse models, comparative biology, and pharmacological interventions.
- Main analysis is qualitative synthesis; no systematic search strategy, inclusion criteria, or meta-analysis is described.
Limitations
- Stated in paper: lack of human tissues and specific markers limits knowledge of senescence in humans; most in vivo evidence comes from laboratory mice, which have known limitations; the exact frequency of senescent cells in older tissues and healthy humans is unknown; causality of senescence in ageing remains debated; and in vivo rates of occurrence and turnover of senescent cells are poorly understood.
- Evident from text: as a narrative review, it does not systematically assess bias or quantify effect sizes, and many cited findings are from mouse models with uncertain translation to humans.
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In the paper
“An emerging body of evidence from animal models, and particularly mice, has demonstrated an important role for senescence in several processes such as embryonic development, wound healing, tumour suppression and ageing.”
§ Stress, cell senescence and organismal ageing > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearThe 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
“It is also now widely accepted that senescence plays a role in vivo.”
§ Stress, cell senescence and organismal ageing > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“During in vitro ageing, the telomeres shorten gradually in each subcultivation (Harley et al., 1990).”
§ Stress, cell senescence and organismal ageing > 2. Of telomeres and senescence
What the sources say
- Not checked yetcites Harley et al., 1990 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Later, pioneering work by Olivier Toussaint and others showed that stress plays a major role in the induction of senescence in vitro, a phenomenon known as stress-induced premature senescence or SIPS.”
§ Stress, cell senescence and organismal ageing > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“With each cell division telomeres shorten progressively, due to the so called “endreplication problem”.”
§ Stress, cell senescence and organismal ageing > 2. Of telomeres and senescence
What the sources say
- Not checked yetcites de Lange, 2005 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Telomere shortening is the key mechanism driving replicative senescence in human fibroblasts.”
- Also stated in: § 2. Of telomeres and senescence · boosted
“Telomere shortening is the primary cause of RS in human fibroblasts, since it has been shown that ectopic expression of telomerase, an enzyme able to counteract telomere shortening, is able to bypass the senescence-induced arrest (Bodnar et al., 1998).”
§ Stress, cell senescence and organismal ageing > Abstract
What the sources say
- Not checked yetcites Bodnar et al., 1998 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § 2. Of telomeres and senescence · boosted
In the paper
“Telomere damage irrespectively of length has also been observed with age in hippocampal neurons and in the liver of baboons (Fumagalli et al., 2012).”
§ Stress, cell senescence and organismal ageing > 3. Is SIPS telomere-independent?
What the sources say
- Not checked yetcites Fumagalli et al., 2012 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“Altogether, these studies suggest that: 1) telomere length is not a limiting factor in an organism's lifespan, and 2) if senescence plays a detrimental role during ageing in vivo (discussed in the next section), this may occur independently of telomere length.”
§ Stress, cell senescence and organismal ageing > 4. The role of telomere-induced senescence in vivo
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Moreover, it was shown that during RS, fibroblasts accumulate proteins involved in the DDR at telomeric regions, including γH2A.X, 53BP1, MDC1 and NBS1 (d'Adda di Fagagna et al., 2003).”
§ Stress, cell senescence and organismal ageing > 2. Of telomeres and senescence
What the sources say
- Not checked yetcites d'Adda di Fagagna et al., 2003 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“It is thought that with each cell division, telomere shortening precipitates the loss of “shelterin” components and the destabilization of the t-loop conformation, resulting in exposure of the telomere end (Griffith et al., 1999).”
§ Stress, cell senescence and organismal ageing > 2. Of telomeres and senescence
What the sources say
- Not checked yetcites Griffith et al., 1999 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- It may state two separate claims as one. 14
- Probably not a substantial claim. 5
In the paper
“As the senescent phenotype develops, most of the DNA damage is repaired within 24 h; however, damage at telomeric regions remains unrepaired for months, contributing to a persistent and unresolved DNA damage response (Hewitt et al., 2012).”
§ Stress, cell senescence and organismal ageing > 3. Is SIPS telomere-independent?
What the sources say
- Not checked yetcites Hewitt et al., 2012 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Inhibition of the JAK pathway (using the drug ruxolitinib) has been shown to suppress the SASP and alleviate age-related tissue dysfunction (Xu et al., 2015).”
§ Stress, cell senescence and organismal ageing > 8. Pharmacological prospects by targeting senescence
What the sources say
- Not checked yetcites Xu et al., 2015
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Induction of SIPS is characterized initially by DNA damage, which occurs randomly all over the genome, and subsequent activation of a DDR.”
§ Stress, cell senescence and organismal ageing > 3. Is SIPS telomere-independent?
What the sources say
- Not checked yetcites Hewitt et al., 2012 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Given the multitude of functions of senescent cells, which can be of a positive or negative nature depending on the context, it has been argued that there may be different types of senescence rather than a universal phenotype.”
§ Stress, cell senescence and organismal ageing > 5. Do senescent cells accumulate with age in tissues?
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
“As mentioned above, senescent cells likely accumulate in some tissues and may contribute to organ dysfunction, yet whether they are causal factors in ageing remains a subject of debate.”
§ Stress, cell senescence and organismal ageing > 7. Genetics of ageing and links to senescence
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“While these results support the idea that telomere shortening is a marker of stress and age-related pathology, they do not prove that telomere shortening is a causal factor in ageing.”
§ Stress, cell senescence and organismal ageing > 4. The role of telomere-induced senescence in vivo
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Further highlighting the potential of targeting senescence as a way to counteract age-related diseases, recent work in mice has shown that genetic elimination of p16-positive senescent cells ameliorated atherosclerosis (Childs et al., 2016) and osteoarthritis (Jeon et al., 2017).”
§ Stress, cell senescence and organismal ageing > 8. Pharmacological prospects by targeting senescence
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Dasatinib and quercetin (D + Q) when given in combination have been shown to reduce senescent cells in aged, radiation-exposed and progeroid mice, improving several healthspan parameters (Zhu et al., 2015).”
§ Stress, cell senescence and organismal ageing > 8. Pharmacological prospects by targeting senescence
What the sources say
- Not checked yetcites Zhu et al., 2015 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Recently, a FOXO4 peptide that perturbs the FOXO4 interaction with p53 was shown to clear senescent cells and improve healthspan in aged and progeroid mice (Baar et al., 2017).”
§ Stress, cell senescence and organismal ageing > 8. Pharmacological prospects by targeting senescence
What the sources say
- Not checked yetcites Baar et al., 2017 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Apart from cell-cycle arrest, senescent cells have been shown to experience dramatic changes in terms of gene expression, metabolism, epigenome and, importantly, have a distinct secretome profile, known as the Senescence-Associated Secretory Phenotype (SASP) (Coppé et al., 2008).”
§ Stress, cell senescence and organismal ageing > 6. Senescent cells can cause tissue disruption and/or degeneration
What the sources say
- Not checked yetcites Coppé et al., 2008 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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, while SIPS induced by sub-lethal acute stress is not driven by the shortening of telomeres per se, in some circumstances SIPS can still be classified as a telomere-dependent process.”
§ Stress, cell senescence and organismal ageing > 3. Is SIPS telomere-independent?
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“DDR activation can result in the activation of transcription factor p53 which is involved in a variety of processes including DNA repair and apoptosis, but most notably results in expression of cyclindependent kinase inhibitor p21, which together with activation of p16, are thought to be the major pathways in the induction of senescence (Beauséjour et al., 2003).”
§ Stress, cell senescence and organismal ageing > 2. Of telomeres and senescence
What the sources say
- Not checked yetcites Beauséjour et al., 2003 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Inhibitors of the BCL-2 family, such as ABT-263 (navitoclax) and ABT-737, have been shown to reduce senescent hematopoietic and muscle stem cells in radiation-exposed and aged mice (Chang et al., 2016) and senescent cells in the lung and epidermis (Yosef et al., 2016).”
§ Stress, cell senescence and organismal ageing > 8. Pharmacological prospects by targeting senescence
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“It has been shown that a “chronic” SASP is able to induce senescence in adjacent young cells, contributing to tissue dysfunction (Acosta et al., 2013;Jurk et al., 2014) and paradoxically tumorigenesis (Krtolica et al., 2001).”
§ Stress, cell senescence and organismal ageing > 6. Senescent cells can cause tissue disruption and/or degeneration
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“For instance, inhibition of the mTOR pathway (using the drug rapamycin), which has been shown to extend lifespan in a variety of model organisms (de Magalhaes et al., 2012;Harrison et al., 2009), is an effective SASP suppressor (Correia-Melo et al., 2016;Herranz et al., 2015;Laberge et al., 2015).”
§ Stress, cell senescence and organismal ageing > 8. Pharmacological prospects by targeting senescence
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“However, given the fact that the SASP is required in certain physiological contexts, it is still unclear whether targeting the SASP would be a viable anti-ageing therapy.”
§ Stress, cell senescence and organismal ageing > 8. Pharmacological prospects by targeting senescence
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
“Finally, we still know very little about in vivo rates of occurrence and turnover of senescent cells.”
§ Stress, cell senescence and organismal ageing > 9. Concluding remarks
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
In the paper
“While our knowledge about senescence in vivo has increased exponentially in the last decade”
§ Stress, cell senescence and organismal ageing > 9. Concluding remarks
What the sources say
- Not checked yetcites de Magalhaes, 2014 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
“it is possible that stress and various insults are contributors to senescence in vivo.”
§ Stress, cell senescence and organismal ageing > 9. Concluding remarks
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
The paper relies on this without support.
Findings from mouse models of senescence and ageing are informative about human ageing.
“In this review, we summarize some of the key findings in the field of senescence, stress-induced senescence and telomeres.We focus particularly on the role of telomere dysfunction and senescence during the ageing process as well as potential interventions, including pharmacological approaches like telomerase activators and senolytics, to counteract their detrimental effects in ageing and disease.”
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?
In the citing paper
“The use of senotherapeutic drugs could potentially be effective in treating a variety of conditions primarily or secondarily mediated by accumulation of senescent cells [6, 33, 67–87].”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [68]
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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.
Conflicting conclusions about telomere length and species longevity
MinorThe paper first says there is no connection between mean telomere length and mammalian species longevity, but later concludes that longevity is strongly associated with the evolution of short telomeres.
“In terms of comparative biology, no connection appears to exist between the mean telomere length of cells and the longevity of mammalian species.”
“Taken together, it seems that the evolution of large body sizes and longevity is strongly associated with the evolution of short telomeres and telomerase suppression, presumably for tumour suppression (de Magalhaes, 2013; Gomes et al., 2011).”
Citations
Cites
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A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
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“…that this view is too simplistic, since senescence has been shown to play multiple important physiological roles, such as: tumour suppression (Serrano et al., 1997), tissue repair and wound healing (Demaria et al., 2014; Krizhanovsky et al., 2008), embryonic development (Muñoz-Espín et al.,…”
InfluentialExtension of Life-Span by Introduction of Telomerase into Normal Human Cells
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“X, 53BP1, MDC1 and NBS1 (d'Adda di Fagagna et al., 2003).”
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Metadata
- Authors
- de Magalhães, J. P., & Passos, J. F.
- Affiliations
- Newcastle University (GB)
- ORCID
- Passos, João F.
- Venue
- Mechanisms of Ageing and Development
- Publisher
- Elsevier BV
- Published
- 2018-03
- Volume
- 170
- Pages
- 2-9
- ISSN
- 0047-6374 (ISSN-L)
- OpenAlex
- W2733273049
- Cited by
- 316
- References
- 122
- Citations by year
- 2026: 17 · 2025: 37 · 2024: 28 · 2023: 31 · 2022: 43 · 2021: 44 · 2020: 55 · 2019: 40 · 2018: 17
- FWCI
- 3.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Mechanisms of Ageing and Development (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity) (cc-by)
- Funders
- Wellcome Trust (104978, 104978/Z/14/Z, RPG-2016-015)
- Methuselah Foundation
- Leverhulme Trust (RPG‐2016‐015)
- Medical Research Council (MR/L016354/1)
- Biotechnology and Biological Sciences Research Council (BB/K017314/1, BB/H022384/1)
- 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 › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- cellular senescence, stress-induced premature senescence, telomere shortening, telomere dysfunction, replicative senescence, senolytics, telomerase activators, tumor suppression, wound healing, embryonic development
- MeSH terms
- Aging, Humans, Neoplasms, Stress, Physiological, Wound Healing, Cellular Senescence, Embryonic Development, Telomere Homeostasis
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