Heart failure and mitochondrial dysfunction: the role of mitochondrial fission/fusion abnormalities and new therapeutic strategies.
Heart failure and mitochondrial dysfunction: the role of mitochondrial fission/fusion abnormalities and new therapeutic strategies.
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DOI：
10.1097/01.fjc.0000432861.55968.a6
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发表时间：
2014-03
影响因子：
3
通讯作者：
Malik ZA
中科院分区：
文献类型：
--
作者：
Knowlton AA;Chen L;Malik ZA
心力衰竭的治疗在过去的三十年中已经发展，认识到神经激素激活及其抑制在改善生活质量和生存率方面的有效性。在过去的20年里，随着新技术的发展，线粒体的研究发生了革命性的变化，发现线粒体以网络连接，甚至在心肌细胞中也进行不断的分裂（裂变）和融合。这导致了心力衰竭中新的分子和细胞发现，这为开发新的基于分子的疗法提供了潜力。活性氧（ROS）是心力衰竭中线粒体和细胞损伤的重要原因，但还有其他异常，如线粒体融合抑制，最终可能成为至少间歇性治疗的目标。线粒体分裂/融合平衡的总体需要可能排除了分裂或融合的持续变化。在这篇综述中，我们将讨论目前的心力衰竭治疗及其对线粒体的影响。此外，我们将审查一些正在开发的新药物靶点。新的分子理解有可能产生有效的新的心力衰竭疗法。
The treatment of heart failure has evolved during the last thirty years with recognition of neurohormonal activation and the effectiveness of its inhibition in improving quality of life and survival. Over the last twenty years there has been a revolution in the investigation of the mitochondrion with the development of new techniques and the finding that mitochondria are connected in networks and undergo constant division (fission) and fusion, even in cardiac myocytes. This has led to new molecular and cellular discoveries in heart failure, which offer the potential for the development of new molecular-based therapies. Reactive oxygen species (ROS) are an important cause of mitochondrial and cellular injury in heart failure, but there are other abnormalities, such as depressed mitochondrial fusion, that may eventually become targets of at least episodic treatment. The overall need for mitochondrial fission/fusion balance may preclude sustained change in either fission or fusion. In this review we will discuss current heart failure therapy and its impact on the mitochondria. In addition we will review some of the new drug targets under development. There is potential for effective, novel therapies for heart failure to arise from new molecular understanding.
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影响因子：
10.8
作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
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作者：
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