Oxidative stress induces an ATM‐independent senescence pathway through p38 MAPK‐mediated lamin B1 accumulation
Open accessAbstract
We report crosstalk between three senescence-inducing conditions, DNA damage response (DDR) defects, oxidative stress (OS) and nuclear shape alterations. The recessive autosomal genetic disorder Ataxia telangiectasia (A-T) is associated with DDR defects, endogenous OS and premature ageing. Here, we find frequent nuclear shape alterations in A-T cells, as well as accumulation of the key nuclear architecture component lamin B1. Lamin B1 overexpression is sufficient to induce nuclear shape alterations and senescence in wild-type cells, and normalizing lamin B1 levels in A-T cells reciprocally reduces both nuclear shape alterations and senescence. We further show that OS increases lamin B1 levels through p38 Mitogen Activated Protein kinase activation. Lamin B1 accumulation and nuclear shape alterations also occur during stress-induced senescence and oncogene-induced senescence (OIS), two canonical senescence situations. These data reveal lamin B1 as a general molecular mediator that controls OS-induced senescence, independent of established Ataxia Telangiectasia Mutated (ATM) roles in OIS.
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Reduction of LMNB1 has been confirmed in various senescent cell types.
“Since then, several studies have confirmed the reduction of LMNB1 in various senescent cell types (Barascu et al. 2012; Freund et al. 2012; Dreesen et al. 2013; Sadaie et al. 2013; Shah et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Barascu et al. 2012
Barascu et al. report the opposite pattern in the cells they studied: the Discussion (p. 12) says persistent oxidative stress causes lamin B1 accumulation that leads to senescence. The A-T cell results (p. 6) further show that reducing lamin B1 decreased the frequency of senescent cells, rather than documenting LMNB1 reduction across senescent cell types. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredOther DNA lesions, such as those from oxidative stress, may also drive senescence.
“Other DNA lesions—such as those caused by oxidative stress—may also drive cells into senescence (35–38).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [35]
The paper’s opening summary (p. 1) identifies oxidative stress as a senescence-inducing condition, and the Discussion (p. 10) describes a pathway by which reactive oxygen species lead to senescence. It does not establish that DNA lesions caused by oxidative stress drive that process; it describes a p38 MAPK–lamin B1 pathway instead. (LLM, conf=0.85)
Experimental — accuracy not yet measuredOxidative stress has been ensured as a crucial factor for cellular senescence through shortening telomere and causing DNA double-strand breaks.
“Oxidative stress has been ensured as a crucial factor for cellular senescence through shortening telomere and causing DNA double-strand breaks.209,210”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [209]
The Introduction (p. 1) and Discussion (p. 10) support oxidative stress as a cause of cellular senescence. They do not establish that it does so by shortening telomeres or causing DNA double-strand breaks; the Discussion instead describes a p38 MAPK–lamin B1 pathway and says A-T cell senescence is not completely due to telomere shortening. (LLM, conf=0.88)
Experimental — accuracy not yet measuredOverexpression of LMNB1 either delays or enhances senescence or exhibits minimal effect on proliferation, depending on study.
“Compared with LMNB1 depletion, phenotypes induced by ectopic LMNB1 were more heterogeneous between studies: Overexpression of LMNB1 either delays (Shimi et al. 2011) or enhances senescence (Barascu et al. 2012; Dreesen et al. 2013) or exhibits a minimal effect on proliferation (Sadaie et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Barascu et al. 2012
Increased levels of LMNB1 are associated with ROS up-regulation and senescence.
“Similarly, Barascu et al. (2012) showed that increased levels of LMNB1 are associated with ROS up-regulation and senescence.”
From Cellular senescence and its effector programs (2014) · cites this paper as Barascu et al. 2012
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- Authors
- Barascu, A., Le Chalony, C., Pennarun, G., Genet, D., Imam, N., Lopez, B., & Bertrand, P.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Bertrand, Pascale
- Venue
- The EMBO Journal
- Published
- 2012-01-13
- Volume
- 31
- Issue
- 5
- Pages
- 1080-1094
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC3297999
- OpenAlex
- W2160703969
- Cited by
- 206
- References
- 84
- Citations by year
- 2026: 6 · 2025: 14 · 2024: 12 · 2023: 8 · 2022: 11 · 2021: 16 · 2020: 17 · 2019: 9 · 2018: 12 · 2017: 12 · 2016: 17 · 2015: 15 · 2014: 24 · 2013: 15 · 2012: 18
- FWCI
- 9.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- The EMBO Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- oxidative stress, cellular senescence, ATM, lamin B1, p38 MAPK, ataxia telangiectasia, DNA damage response, stress-induced senescence, oncogene-induced senescence, nuclear organization, premature aging
- MeSH terms
- Aging, Cells, Cultured, Humans, Signal Transduction, Oxidative Stress, Lamin Type B, p38 Mitogen-Activated Protein Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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