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Hallmarks of cellular senescence: biology, mechanisms, regulations
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Journal Article
Hallmarks of cellular senescence: biology, mechanisms, regulations
2025
Overview
Cellular senescence is a process in which the cell cycle becomes permanently arrested, thereby inhibiting cell division, proliferation and growth. Various cellular stresses, such as DNA damage, telomere shortening and oxidative stress, can trigger cellular senescence. Physiologically, cellular senescence contributes to tissue development, repair and critical biological processes such as embryogenesis, whereas, pathologically, it plays a key role in diverse disease subsets. To this end, elucidating the underlying mechanisms and molecular regulation of senescence is crucial. Here, in this Review, we explore recent key findings on cellular senescence in experimental and human disease models, focusing on its molecular mechanisms, regulation and future research directions to advance the field and facilitate therapeutic translation.
Cellular senescence mechanisms impacting health and disease
Cellular senescence is a natural process in which cells stop dividing in response to stress, such as DNA damage. However, it can also contribute to diseases such as idiopathic pulmonary fibrosis (IPF), a lung condition with unknown causes. Researchers found that a protein called YTHDC1 can delay cellular senescence and reduce lung fibrosis by improving DNA repair in cells. They studied this in mice and found that increasing YTHDC1 levels helped to repair DNA and reduced fibrosis. The study used experimental methods to overexpress YTHDC1 in mouse lung cells, showing its potential to reverse senescence. The results suggest that targeting YTHDC1 could be a new way to treat IPF. However, more research is needed to confirm these findings and explore their safety in humans. In conclusion, understanding cellular senescence’s role in diseases such as IPF could lead to new treatments.
This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.
