Tang Ying, Liu Jiankang, Long Jiangang
Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology and Frontier Institute of Life Science, FIST, Xi'an Jiaotong University Xi'an, China.
J Diabetes Investig. 2015 May;6(3):250-5. doi: 10.1111/jdi.12302. Epub 2014 Dec 16.
Diabetes is an independent risk factor for cardiovascular morbidity and mortality. Diabetes-associated cardiac pathophysiology is recognized to be due to reasons including metabolic consequences on the myocardium. The heart is a highly energy-demanding tissue, with mitochondria supplying over 90% of adenosine triphosphate. The involvement of mitochondrial dysfunction in diabetes-related cardiac pathogenesis has been studied. Phosphatase and tensin homolog-induced putative kinase 1 (PINK1) and Parkin, initially identified to be associated with the pathogenesis of a familiar form of Parkinson's disease, have recently been recognized to play a critical role in mediating cardiomyocytes' adaption to stresses. Extensive studies have suggested PINK1 and Parkin as key regulators of mitophagy. In the present review article, we will first summarize the new findings on PINK1/Parkin acting in cardioprotection, and then discuss the potential role of PINK1/Parkin in diabetic heart by mediating mitophagy.
糖尿病是心血管疾病发病和死亡的独立危险因素。糖尿病相关的心脏病理生理学被认为是由包括心肌代谢后果在内的多种原因引起的。心脏是一个高能量需求的组织，线粒体提供超过90%的三磷酸腺苷。线粒体功能障碍在糖尿病相关心脏发病机制中的作用已得到研究。磷酸酶和张力蛋白同源物诱导的假定激酶1（PINK1）和帕金蛋白，最初被确定与一种常见形式的帕金森病发病机制有关，最近被认为在介导心肌细胞对压力的适应中起关键作用。大量研究表明PINK1和帕金蛋白是线粒体自噬的关键调节因子。在本综述文章中，我们将首先总结PINK1/帕金蛋白在心脏保护作用方面的新发现，然后讨论PINK1/帕金蛋白通过介导线粒体自噬在糖尿病心脏中的潜在作用。
