Journal
JOURNAL OF BIOCHEMISTRY
Volume 169, Issue 2, Pages 147-153Publisher
OXFORD UNIV PRESS
DOI: 10.1093/jb/mvaa109
Keywords
cellular senescence; cGAS-STING; DNA damage; extracellular vesicle; senescence-associated secretory phenotype
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Funding
- Agency for Medical Research and Development (AMED) [17cm0106202h0002]
- Advanced Research & Development Programs for Medical Innovation (PRIME) [19gm6110023h0001]
- Japan Science and Technology Agency (JST)/Precursory Research for Embryonic Science and Technology (PRESTO) [JPMJPR17H7]
- Japan Society for the Promotion of Science (JSPS) [18K15073, 19H03507]
- Grants-in-Aid for Scientific Research [19H03507, 18K15073] Funding Source: KAKEN
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Cellular senescence serves as an important tumor suppression mechanism by inhibiting the proliferation of damaged cells. Irreparable DNA damage in senescent cells leads to the accumulation of genomic DNA fragments in the cytoplasm, triggering the secretion of inflammatory proteins and increasing the release of small extracellular vesicles. This phenomenon, known as senescence-associated secretory phenotype, plays a role in various physiological and pathological processes in the body.
Cellular senescence is an important tumour suppression mechanism that inhibits the proliferation of damaged cells. In senescent cells, irreparable DNA damage causes accumulation of genomic DNA fragments in the cytoplasm, which are recognized by the cyclic GMP-AMP synthase-stimulator of interferon gene pathway, resulting in secretion of numerous inflammatory proteins. This phenomenon is called senescence-associated secretory phenotype, and results in multiple physiological or pathological processes in the body. In addition, DNA damage also increases small extracellular vesicle release from senescent cells. This review presents recent insights into the molecular mechanisms and biological functions of senescence-associated extracellular vesicle release that is associated with age-related diseases, particularly cancer.
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