1. The role of RhoA-ROCK signaling in benign prostatic hyperplasia: a review.
- Author
-
Shan S and Su M
- Subjects
- Humans, Male, Prostate pathology, Prostate metabolism, Cell Proliferation genetics, Apoptosis genetics, Muscle, Smooth metabolism, Muscle, Smooth pathology, Risk Factors, Muscle Contraction physiology, Fibrosis, Prostatic Hyperplasia metabolism, Prostatic Hyperplasia etiology, rho-Associated Kinases metabolism, rho-Associated Kinases physiology, rhoA GTP-Binding Protein metabolism, rhoA GTP-Binding Protein physiology, Signal Transduction physiology, Signal Transduction genetics
- Abstract
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
2+ 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., Competing Interests: Declarations. Conflict of interest: The authors declare that there is no conflict of interest. Institutional review board statement: Not applicable. Informed consent statement: Not applicable., (© 2025. The Author(s) under exclusive licence to Japan Human Cell Society.)- Published
- 2025
- Full Text
- View/download PDF