» Articles » PMID: 34294916

Cellular Senescence As a Possible Link Between Prostate Diseases of the Ageing Male

Overview
Journal Nat Rev Urol
Specialty Urology
Date 2021 Jul 23
PMID 34294916
Citations 22
Authors
Affiliations
Soon will be listed here.
Abstract

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.

Citing Articles

Sestrin2 ameliorates age-related spontaneous benign prostatic hyperplasia via activation of AMPK/mTOR dependent autophagy.

Lee H, Kim Y, Park H, Kim H, Kim H, Hong G Biogerontology. 2025; 26(1):48.

PMID: 39853471 DOI: 10.1007/s10522-025-10184-4.


Prostatitis, benign prostatic hyperplasia, and prostate cancer: a bidirectional Mendelian randomization study and clinical implications for these patients' populations.

Wang Y, Chen G, Li D, Zhang D, Xing Q Biol Direct. 2024; 19(1):129.

PMID: 39695756 PMC: 11658280. DOI: 10.1186/s13062-024-00575-x.


Association of biological aging with prostate cancer: insights from the National Health and Nutrition Examination Survey.

Yin W, Song B, Yu C, Jiang J, Yan Z, Xie C Aging Clin Exp Res. 2024; 36(1):209.

PMID: 39446214 PMC: 11502538. DOI: 10.1007/s40520-024-02861-0.


Autophagy in benign prostatic hyperplasia: insights and therapeutic potential.

Zhou X, Huang P, Wu Y, Yu J, Sun J BMC Urol. 2024; 24(1):198.

PMID: 39261818 PMC: 11391623. DOI: 10.1186/s12894-024-01585-7.


Identification of circadian clock-related immunological prognostic index and molecular subtypes in prostate cancer.

Che L, Li D, Wang J, Tuo Z, Yoo K, Feng D Discov Oncol. 2024; 15(1):429.

PMID: 39259370 PMC: 11391008. DOI: 10.1007/s12672-024-01276-7.


References
1.
Berry S, Coffey D, Walsh P, EWING L . The development of human benign prostatic hyperplasia with age. J Urol. 1984; 132(3):474-9. DOI: 10.1016/s0022-5347(17)49698-4. View

2.
Soos G, Tsakiris I, Szanto J, Turzo C, Haas P, Dezso B . The prevalence of prostate carcinoma and its precursor in Hungary: an autopsy study. Eur Urol. 2005; 48(5):739-44. DOI: 10.1016/j.eururo.2005.08.010. View

3.
Bell K, Del Mar C, Wright G, Dickinson J, Glasziou P . Prevalence of incidental prostate cancer: A systematic review of autopsy studies. Int J Cancer. 2015; 137(7):1749-57. PMC: 4682465. DOI: 10.1002/ijc.29538. View

4.
McNeal J . The zonal anatomy of the prostate. Prostate. 1981; 2(1):35-49. DOI: 10.1002/pros.2990020105. View

5.
McNeal J, Redwine E, Freiha F, Stamey T . Zonal distribution of prostatic adenocarcinoma. Correlation with histologic pattern and direction of spread. Am J Surg Pathol. 1988; 12(12):897-906. DOI: 10.1097/00000478-198812000-00001. View