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.
The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.
Research summary
The paper discusses the mechanisms of cellular senescence and their contributions to ageing and age-related diseases, focusing on underlying biological processes such as chromatin dynamics and genome instability. This aligns with longevity research as it addresses root causes of ageing rather than merely treating symptoms. The proposed therapeutic strategies to counteract cellular senescence are significant, but the review nature of the paper limits its impact to an important contribution rather than a groundbreaking one.
Author of this paper? Send a correction.