Molecular mechanism of ubiquitination modification in pulmonary hy-pertension
10.3969/j.issn.1000-4718.2025.08.023
- VernacularTitle:泛素化修饰调控肺动脉高压的分子机制
- Author:
Qihao SHI
1
;
Yiting DONG
;
Chendong WU
;
Linbo YUAN
Author Information
1. 温州医科大学第二临床医学院,浙江 温州 325000
- Publication Type:Journal Article
- Keywords:
pulmonary hypertension;
ubiquitination;
proteasomes
- From:
Chinese Journal of Pathophysiology
2025;41(8):1646-1651
- CountryChina
- Language:Chinese
-
Abstract:
Pulmonary hypertension(PH)is a serious cardiovascular condition that significantly impacts pa-tients'quality of life.Currently available clinical medications lack selectivity for pulmonary blood vessels,often produce substantial side effects,and are prohibitively expensive.Therefore,it is crucial to explore the mechanisms underlying the onset and progression of PH and to develop new,effective treatments.Ubiquitination is a key form of protein post-transla-tional modification in which specific E3 enzymes recognize substrate proteins and induce ubiquitination,leading to chang-es in their activity or stability.During the onset of PH,the activities of ubiquitin ligases and deubiquitinases undergo vari-ous changes,resulting in altered ubiquitination levels of different proteins.These variations primarily influence the degra-dation rates of substrate proteins within cells,thereby regulating essential physiological processes.Proteasomes play a vi-tal role in the degradation of ubiquitinated proteins,and inhibitors targeting these complexes have been developed,demon-strating therapeutic efficacy in experimental settings of PH.However,their low specificity presents significant challenges for practical applications.In this context,we summarize the relevant mechanisms of ubiquitination regulation in the onset of PH and highlight its practical significance for future therapeutic strategies.
