Mitochondrial shaping proteins as novel treatment targets for cardiomyopathies.
Mitochondrial shaping proteins as novel treatment targets for cardiomyopathies.
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发表时间：
2020-08
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通讯作者：
S. Kalkhoran;S. Hernandez-Resendiz;S. Ong;C. Ramachandra;D. Hausenloy
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作者：
S. Kalkhoran;S. Hernandez-Resendiz;S. Ong;C. Ramachandra;D. Hausenloy
心力衰竭是世界范围内导致死亡和残疾的主要原因之一。心力衰竭的患病率继续上升，其结果因年龄、糖尿病、肥胖、高血压和缺血性心脏病等危险因素而恶化。因此，有一个尚未得到满足的需要，以确定新的治疗目标，以防止心力衰竭的发展和进展，以改善患者的结果。在这一点上，心肌线粒体在产生维持正常心脏收缩功能所需的三磷酸腺苷方面起着至关重要的作用。线粒体功能障碍被认为是许多心肌疾病的发病机制之一，包括继发性糖尿病、压力超负荷性左心室肥厚(LVH)和阿霉素心脏毒性。线粒体通过融合和分裂不断改变其形状，线粒体融合和分裂的不平衡影响了线粒体的功能，并参与了这些心肌病的发病。在这篇综述文章中，我们重点讨论线粒体形成蛋白在三种心肌病的发生发展中的作用，并强调它们作为预防心力衰竭发生和发展的新的治疗靶点的潜力。
Heart failure (HF) is one of the leading causes of death and disability worldwide. The prevalence of HF continues to rise, and its outcomes are worsened by risk factors such as age, diabetes, obesity, hypertension, and ischemic heart disease. Hence, there is an unmet need to identify novel treatment targets that can prevent the development and progression of HF in order to improve patient outcomes. In this regard, cardiac mitochondria play an essential role in generating the ATP required to maintain normal cardiac contractile function. Mitochondrial dysfunction is known to contribute to the pathogenesis of a number of cardiomyopathies including those secondary to diabetes, pressure-overload left ventricular hypertrophy (LVH), and doxorubicin cardiotoxicity. Mitochondria continually change their shape by undergoing fusion and fission, and an imbalance in mitochondrial fusion and fission have been shown to impact on mitochondrial function, and contribute to the pathogenesis of these cardiomyopathies. In this review article, we focus on the role of mitochondrial shaping proteins as contributors to the development of three cardiomyopathies, and highlight their therapeutic potential as novel treatment targets for preventing the onset and progression of HF.