Mitochondrial therapeutics for cardioprotection.
Mitochondrial therapeutics for cardioprotection.
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DOI：
10.2174/138161211796904777
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发表时间：
2011
影响因子：
3.1
通讯作者：
Gottlieb RA
中科院分区：
文献类型：
--
作者：
Carreira RS;Lee P;Gottlieb RA
线粒体约占心脏质量的三分之一，在维持细胞功能方面起着至关重要的作用，然而，它们也是自由基和促凋亡因子的有力来源。因此，维持线粒体稳态对细胞存活至关重要。作为ATP的主要来源，持续的质量控制是保证其持续优化功能的必要条件。线粒体质量控制是通过融合、裂变、自噬和线粒体生物发生的动态相互作用来完成的。这篇综述探讨了心脏中的这些过程，并考虑了它们在缺血再灌注损伤中的作用。本文讨论了调节线粒体更新的干预措施，包括药物、运动和热量限制，作为改善线粒体质量控制、改善心血管功能障碍和延长寿命的手段。
Mitochondria represent approximately one-third of the mass of the heart and play a critical role in maintaining cellular function—however, they are also a potent source of free radicals and pro-apoptotic factors. As such, maintaining mitochondrial homeostasis is essential to cell survival. As the dominant source of ATP, continuous quality control is mandatory to ensure their ongoing optimal function. Mitochondrial quality control is accomplished by the dynamic interplay of fusion, fission, autophagy, and mitochondrial biogenesis. This review examines these processes in the heart and considers their role in the context of ischemia-reperfusion injury. Interventions that modulate mitochondrial turnover, including pharmacologic agents, exercise, and caloric restriction are discussed as a means to improve mitochondrial quality control, ameliorate cardiovascular dysfunction, and enhance longevity.