Marín-García José, Goldenthal Michael J
The Molecular Cardiology and Neuromuscular Institute, 75 Raritan Ave., Highland Park, NJ 08904, USA.
Heart Fail Rev. 2008 Jun;13(2):137-50. doi: 10.1007/s10741-007-9079-1. Epub 2008 Jan 5.
A number of observations have shown that mitochondria are at the center of the pathophysiology of the failing heart and mitochondrial-based oxidative stress (OS), myocardial apoptosis, and cardiac bioenergetic dysfunction are implicated in the progression of heart failure (HF), as shown by both clinical studies and animal models. In this manuscript, we review the body of evidence that multiple defects in mitochondria are central and primary to HF progression. In addition, novel approaches to therapeutic targeting of mitochondrial bioenergetic, biogenic, and signaling abnormalities that can impact HF are discussed.
大量观察结果表明，线粒体处于衰竭心脏病理生理学的核心位置，临床研究和动物模型均显示，基于线粒体的氧化应激（OS）、心肌细胞凋亡以及心脏生物能量功能障碍与心力衰竭（HF）的进展有关。在本手稿中，我们综述了一系列证据，这些证据表明线粒体的多种缺陷是HF进展的核心和主要因素。此外，还讨论了针对线粒体生物能量、生物发生和信号异常进行治疗靶向的新方法，这些异常可能会影响HF。
