线粒体动力学稳态是由连续和平衡的裂变和融合维持的，它们是形态的决定因素，丰度,线粒体的生物发生和线粒体自噬。视神经萎缩1（OPA1），作为唯一的线粒体内膜融合蛋白，在稳定线粒体动力学中起关键作用。线粒体动力学的紊乱有助于心血管疾病的病理生理进展，是近几十年来世界范围内死亡的主要原因，并造成巨大的社会负担。在这次审查中,我们描述了关于OPA1及其在线粒体融合中的作用的最新发现.我们总结了OPA1的翻译后修饰（PTM）及其在线粒体动力学中的调节作用。然后讨论了心血管疾病期间由OPA1表达引起的各种细胞命运。此外，心血管疾病（如心力衰竭，心肌缺血/再灌注损伤,心肌病和心脏肥大）与OPA1依赖性线粒体动力学失衡有关。最后,我们强调了靶向OPA1影响线粒体融合的潜力,这可能被用作抗心血管疾病的新策略.
Mitochondrial dynamics homeostasis is sustained by continuous and balanced fission and fusion, which are determinants of morphology, abundance, biogenesis and mitophagy of mitochondria. Optic atrophy 1 (OPA1), as the only inner mitochondrial membrane fusion protein, plays a key role in stabilizing mitochondrial dynamics. The disturbance of mitochondrial dynamics contributes to the pathophysiological progress of cardiovascular disorders, which are the main cause of death worldwide in recent decades and result in tremendous social burden. In this
review, we describe the latest findings regarding OPA1 and its role in mitochondrial fusion. We summarize the post-translational modifications (PTMs) for OPA1 and its regulatory role in mitochondrial dynamics. Then the diverse cell fates caused by OPA1 expression during cardiovascular disorders are discussed. Moreover, cardiovascular disorders (such as heart failure, myocardial ischemia/reperfusion injury, cardiomyopathy and cardiac hypertrophy) relevant to OPA1-dependent mitochondrial dynamics imbalance have been detailed. Finally, we highlight the potential that targeting OPA1 to impact mitochondrial fusion may be used as a novel strategy against cardiovascular disorders.
