Xiong Zhenyu, Liao Yuanpeng, Zhang Zhaoshan, Wan Zhengdong, Liang Sijia, Guo Jiawei
Department of Vascular and Endovascular Surgery, The First Affiliated Hospital of Yangtze University, Jingzhou 434000, China.
Department of Pharmacology, School of Medicine, Yangtze University, Jingzhou 434023, China.
Biomolecules. 2025 May 6;15(5):670. doi: 10.3390/biom15050670.
Cardiomyopathies comprise a heterogeneous group of cardiac disorders characterized by structural and functional abnormalities in the absence of significant coronary artery disease, hypertension, valvular disease, or congenital defects. Major subtypes include hypertrophic, dilated, arrhythmogenic, and stress-induced cardiomyopathies. Oxidative stress (OS), resulting from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, has emerged as a key contributor to the pathogenesis of these conditions. ROS-mediated injury drives inflammation, protease activation, mitochondrial dysfunction, and cardiomyocyte damage, thereby promoting cardiac remodeling and functional decline. Although numerous studies implicate OS in cardiomyopathy progression, the precise molecular mechanisms remain incompletely defined. This review provides an updated synthesis of current findings on OS-related signaling pathways across cardiomyopathy subtypes, emphasizing emerging therapeutic targets within redox-regulatory networks. A deeper understanding of these mechanisms may guide the development of targeted antioxidant strategies to improve clinical outcomes in affected patients.
心肌病是一组异质性心脏疾病，其特征是在无显著冠状动脉疾病、高血压、瓣膜病或先天性缺陷的情况下出现结构和功能异常。主要亚型包括肥厚型、扩张型、致心律失常型和应激性心肌病。氧化应激（OS）是由于活性氧（ROS）产生与抗氧化防御之间的失衡所致，已成为这些疾病发病机制的关键因素。ROS介导的损伤会引发炎症、蛋白酶激活、线粒体功能障碍和心肌细胞损伤，从而促进心脏重塑和功能衰退。尽管众多研究表明氧化应激与心肌病进展有关，但其确切的分子机制仍未完全明确。本综述对当前关于各心肌病亚型中与氧化应激相关信号通路的研究结果进行了更新总结，强调了氧化还原调节网络中新出现的治疗靶点。对这些机制的更深入理解可能会指导有针对性的抗氧化策略的开发，以改善受影响患者的临床结局。
