Department of Angiocardioneurology, IRCCS Neuromed, Località Camerelle, 86077, Pozzilli, IS, Italy.
Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University of Rome, Ospedale S. Andrea, Rome, Italy.
J Mol Med (Berl). 2019 May;97(5):579-591. doi: 10.1007/s00109-019-01771-3. Epub 2019 Mar 12.
Compelling evidence demonstrates the emerging role of mitochondrial complex I deficiency in the onset and development of cardiovascular diseases (CVDs). In particular, defects in single subunits of mitochondrial complex I have been associated with cardiac hypertrophy, ischemia/reperfusion injury, as well as diabetic complications and stroke in pre-clinical studies. Moreover, data obtained in humans revealed that genes coding for complex I proteins were associated with different CVDs. In this review, we discuss recent experimental studies that underline the contributory role of mitochondrial complex I deficiency in the etiopathogenesis of several CVDs, with a particular focus on those involving loss of function models of mitochondrial complex I. We also discuss human studies and potential therapeutic strategies able to rescue mitochondrial function in CVDs.
大量证据表明，线粒体复合物 I 缺陷在心血管疾病 (CVDs) 的发生和发展中起着重要作用。特别是，线粒体复合物 I 单个亚基的缺陷与心脏肥大、缺血/再灌注损伤以及临床前研究中的糖尿病并发症和中风有关。此外，在人类中获得的数据表明，编码复合物 I 蛋白的基因与不同的 CVDs 有关。在这篇综述中，我们讨论了最近的实验研究，这些研究强调了线粒体复合物 I 缺陷在几种 CVD 的发病机制中的贡献作用，特别关注涉及线粒体复合物 I 功能丧失模型的研究。我们还讨论了能够挽救 CVD 中线粒体功能的人类研究和潜在治疗策略。
