衰老
前列腺癌
前列腺
表型
老化
机制(生物学)
癌症研究
炎症
癌症
细胞生物学
免疫学
生物
遗传学
基因
认识论
哲学
作者
G. Fiard,Vasilis Stavrinides,Emma S. Chambers,Susan Heavey,Alex Freeman,Rhys Ball,Arne N. Akbar,Mark Emberton
标识
DOI:10.1038/s41585-021-00496-8
摘要
Senescent cells accumulate with age in all tissues. Although senescent cells undergo cell-cycle arrest, these cells remain metabolically active and their secretome — known as the senescence-associated secretory phenotype — is responsible for a systemic pro-inflammatory state, which contributes to an inflammatory microenvironment. Senescent cells can be found in the ageing prostate and the senescence-associated secretory phenotype and can be linked to BPH and prostate cancer. Indeed, a number of signalling pathways provide biological plausibility for the role of senescence in both BPH and prostate cancer, although proving causality is difficult. The theory of senescence as a mechanism for prostate disease has a number of clinical implications and could offer opportunities for targeting in the future. Senescent cells and their secretome — the senescence-associated secretory phenotype (SASP) — cause a systemic pro-inflammatory state, contributing to an inflammatory microenvironment. In this article, the authors discuss the presence of senescent cells and the SASP in the ageing prostate and the evidence for a role of senescence in BPH and prostate cancer, as well as possible therapeutic targeting of these pathways in the future.
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