线粒体作为心力衰竭的治疗靶点。
Mitochondria as a therapeutic target in heart failure.
机构信息
Feinberg Cardiovascular Research Institute, Northwestern University School of Medicine, Chicago, Illinois, USA.
出版信息
J Am Coll Cardiol. 2013 Feb 12;61(6):599-610. doi: 10.1016/j.jacc.2012.08.1021. Epub 2012 Dec 5.
Abstract
Heart failure is a pressing public health problem with no curative treatment currently available. The existing therapies provide symptomatic relief, but are unable to reverse molecular changes that occur in cardiomyocytes. The mechanisms of heart failure are complex and multiple, but mitochondrial dysfunction appears to be a critical factor in the development of this disease. Thus, it is important to focus research efforts on targeting mitochondrial dysfunction in the failing heart to revive the myocardium and its contractile function. This review highlights the 3 promising areas for the development of heart failure therapies, including mitochondrial biogenesis, mitochondrial oxidative stress, and mitochondrial iron handling. Moreover, the translational potential of compounds targeting these pathways is discussed.
摘要
心力衰竭是一个紧迫的公共卫生问题，目前尚无治愈方法。现有的治疗方法只能提供症状缓解，而不能逆转心肌细胞中发生的分子变化。心力衰竭的机制复杂多样，但线粒体功能障碍似乎是该疾病发展的关键因素。因此，重要的是要集中研究心力衰竭中心肌细胞线粒体功能障碍的靶向治疗，以恢复心肌及其收缩功能。这篇综述强调了心力衰竭治疗发展的 3 个有前途的领域，包括线粒体生物发生、线粒体氧化应激和线粒体铁处理。此外，还讨论了针对这些途径的化合物的转化潜力。
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