Shan Shidong, Su Min
Department of Renal Transplantation, Guangdong Provincial People' Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Hum Cell. 2025 Feb 1;38(2):48. doi: 10.1007/s13577-025-01179-x.
Benign prostatic hyperplasia (BPH) is a common urological disease in middle-aged and elderly men. The main pathological mechanisms of BPH include static factors that increase prostate volume and dynamic factors that increase prostate tension. The RhoA/ROCK signaling pathway is a classical pathway that regulates cell contraction, migration, and growth. In this review, we summarize the potential role of RhoA/ROCK signaling in the development of BPH. The RhoA/ROCK signaling pathway can enhance the contraction of prostate smooth muscle through the Ca sensitization pathway and increase passive tension in the prostate through tissue fibrosis. Additionally, RhoA/ROCK signaling promotes cell proliferation by regulating cell division and may influence apoptosis by affecting the actin cytoskeleton. Furthermore, risk factors, such as inflammation, metabolic syndrome, and hormonal changes, can upregulate RhoA/ROCK signaling, which in turn promotes these risk factors, eventually leading to the development of BPH. Given the role of RhoA/ROCK signaling in regulating multiple pathogenic factors of BPH, this pathway represents a promising molecular target for BPH treatment and warrants further study.
良性前列腺增生（BPH）是中老年男性常见的泌尿系统疾病。BPH的主要病理机制包括增加前列腺体积的静态因素和增加前列腺张力的动态因素。RhoA/ROCK信号通路是调节细胞收缩、迁移和生长的经典通路。在本综述中，我们总结了RhoA/ROCK信号在BPH发生发展中的潜在作用。RhoA/ROCK信号通路可通过钙敏化途径增强前列腺平滑肌的收缩，并通过组织纤维化增加前列腺的被动张力。此外，RhoA/ROCK信号通过调节细胞分裂促进细胞增殖，并可能通过影响肌动蛋白细胞骨架影响细胞凋亡。此外，炎症、代谢综合征和激素变化等危险因素可上调RhoA/ROCK信号，进而促进这些危险因素，最终导致BPH的发生。鉴于RhoA/ROCK信号在调节BPH多种致病因素中的作用，该通路是BPH治疗有前景的分子靶点，值得进一步研究。
