Ketenci Melis, Zablocki Daniela, Sadoshima Junichi
Rutgers New Jersey Medical School, Department of Cell Biology and Molecular Medicine, Rutgers Biomedical and Health Sciences, Newark, USA.
JMA J. 2022 Oct 17;5(4):407-415. doi: 10.31662/jmaj.2022-0155. Epub 2022 Sep 30.
One of the major complications of diabetes mellitus is diabetic cardiomyopathy. One of the mechanisms that initiates the irreversible deterioration of cardiac function in diabetic cardiomyopathy is mitochondrial dysfunction. Functionally impaired mitochondria result in greater levels of oxidative stress and lipotoxicity, both of which exacerbate mitochondrial damage. Mitochondrial health is constantly monitored by mitochondrial quality control mechanisms. Mitophagy selectively degrades damaged mitochondria, thereby maintaining the healthy pool of mitochondria and preserving myocardial function. Mitophagy in diabetic cardiomyopathy is mediated by multiple mechanisms in a time-dependent manner. Potential targets for the treatment of diabetic cardiomyopathy include increased oxidative stress, mitochondrial dynamics, and mitochondrial clearance. Thus, stimulation of mitophagy represents a promising strategy for the alleviation of diabetic cardiomyopathy.
糖尿病的主要并发症之一是糖尿病性心肌病。引发糖尿病性心肌病中心脏功能不可逆恶化的机制之一是线粒体功能障碍。功能受损的线粒体导致更高水平的氧化应激和脂毒性，这两者都会加剧线粒体损伤。线粒体质量控制机制会持续监测线粒体的健康状况。线粒体自噬选择性地降解受损线粒体，从而维持线粒体的健康库并保护心肌功能。糖尿病性心肌病中的线粒体自噬由多种机制以时间依赖性方式介导。治疗糖尿病性心肌病的潜在靶点包括增加氧化应激、线粒体动力学和线粒体清除。因此，刺激线粒体自噬是缓解糖尿病性心肌病的一种有前景的策略。
