Cellular senescence as a possible link between prostate diseases of the ageing male

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. 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.

Automated summary

Senescent cells and the SASP play a significant role in prostate aging, potentially linked to BPH and prostate cancer.