Zhang Yu, Yang Jiahui, Min Jiali, Huang Shan, Li Yuchen, Liu Shanshan
National Clinical Research Center for Metabolic Diseases, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, CSU-Sinocare Research Center for Nutrition and Metabolic Health, Furong Laboratory, Changsha, Hunan, 410011, China.
J Transl Med. 2025 Mar 25;23(1):368. doi: 10.1186/s12967-025-06255-2.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease worldwide, with a prevalence as high as 32.4%. MASLD encompasses a spectrum of liver pathologies, ranging from steatosis to metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, and, in some cases, progression to end-stage liver disease (cirrhosis and hepatocellular carcinoma). A comprehensive understanding of the pathogenesis of this highly prevalent liver disease may facilitate the identification of novel targets for the development of improved therapies. E3 ubiquitin ligases and deubiquitinases (DUBs) are key regulatory components of the ubiquitin‒proteasome system (UPS), which plays a pivotal role in maintaining intracellular protein homeostasis. Emerging evidence implicates that aberrant expression of E3 ligases and DUBs is involved in the progression of MASLD. Here, we review abnormalities in E3 ligases and DUBs by (1) discussing their targets, mechanisms, and functions in MASLD; (2) summarizing pharmacological interventions targeting these enzymes in preclinical and clinical studies; and (3) addressing challenges and future therapeutic strategies. This review synthesizes current evidence to highlight the development of novel therapeutic strategies based on the UPS for MASLD and progressive liver disease.
代谢功能障碍相关脂肪性肝病(MASLD)是全球最常见的慢性肝病,患病率高达32.4%。MASLD涵盖一系列肝脏病变,从脂肪变性到代谢功能障碍相关脂肪性肝炎(MASH)、纤维化,在某些情况下还会进展为终末期肝病(肝硬化和肝细胞癌)。全面了解这种高度流行的肝病的发病机制可能有助于确定开发改进疗法的新靶点。E3泛素连接酶和去泛素化酶(DUBs)是泛素-蛋白酶体系统(UPS)的关键调节成分,该系统在维持细胞内蛋白质稳态中起关键作用。新出现的证据表明,E3连接酶和DUBs的异常表达与MASLD的进展有关。在这里,我们通过(1)讨论它们在MASLD中的靶点、机制和功能;(2)总结临床前和临床研究中针对这些酶的药物干预措施;(3)应对挑战和未来的治疗策略,来综述E3连接酶和DUBs的异常情况。本综述综合了当前的证据,以突出基于UPS针对MASLD和进行性肝病开发新治疗策略的情况。