Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases
Abstract
Ageing is a complex biological process in which a gradual decline in physiological fitness increases susceptibility to diseases such as neurodegenerative disorders and cancer. Cellular senescence, a state of irreversible cell-growth arrest accompanied by functional deterioration, has emerged as a pivotal driver of ageing. In this Review, we discuss how heterochromatin loss, telomere attrition and DNA damage contribute to cellular senescence, ageing and age-related diseases by eliciting genome instability, innate immunity and inflammation. We also discuss how emerging therapeutic strategies could restore heterochromatin stability, maintain telomere integrity and boost the DNA repair capacity, and thus counteract cellular senescence and ageing-associated pathologies. Finally, we outline current research challenges and future directions aimed at better comprehending and delaying ageing.
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IgG induces senescence in macrophages derived from bone marrow, spleen, and peritoneal cavity, as indicated by increased SA-β-Gal activity, P21 expression, upregulated MMTV-positive cells, aggresome formation, and decreased H3K9me3 and lamin B1 levels.
“Our data revealed that IgG induced senescence in these macrophages, as indicated by an increase in SA-β-Gal activity and P21 expression, along with upregulated MMTV-positive cells, aggresome formation, and decreased H3K9me3 and lamin B1 levels46”
From Spatial transcriptomic landscape unveils immunoglobin-associated senescence as a hallmark of aging (2024) · cites this paper as [46]
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Spatial transcriptomic landscape unveils immunoglobin-associated senescence as a hallmark of aging
Ma, S., Ji, Z., Zhang, B., Geng, L., Cai, Y., Nie, C., Li, J., Zuo, Y., Sun, Y., Xu, G., et al. (2024) · Cell · doi:10.1016/j.cell.2024.10.019 · Cited by 162 · see citing works
Self-citation
- Authors
- Wu, Z., Qu, J., & Liu, G.-H.
- Affiliations
- Chinese Academy of Sciences (CN)
- Capital Medical University (CN)
- Corresponding author
- Qu, Jing
- Liu, Guang-Hui
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2024-10-03
- Volume
- 25
- Issue
- 12
- Pages
- 979-1000
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- OpenAlex
- W4403099207
- Cited by
- 118
- References
- 66
- Citations by year
- 2026: 64 · 2025: 48 · 2024: 6
- FWCI
- 6.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- cellular senescence, aging, heterochromatin loss, telomere shortening, DNA damage, genomic instability, innate immunity, inflammation, age-related diseases, DNA repair, neurodegenerative diseases, cancer
- MeSH terms
- Aging, Animals, Chromatin, DNA Damage, DNA Repair, Heterochromatin, Humans, Telomere, Cellular Senescence, Neurodegenerative Diseases, Genomic Instability
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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