Mitophagy and heart failure.

Mitophagy and heart failure.
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线粒体自噬与心力衰竭。

DOI:
10.1007/s00109-015-1254-6
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发表时间:
2015-03
影响因子:
4.7
通讯作者:
Gustafsson, Asa B.
Gustafsson, Asa B.
中科院分区:
医学2区
文献类型:
--
作者:
Shires, Sarah E.;Gustafsson, Asa B.

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心脏线粒体负责通过氧化磷酸化以ATP的形式产生能量,并且对心脏功能至关重要。线粒体功能障碍是心肌细胞损失和心力衰竭发展的主要原因。肌细胞具有适当的质量控制机制,以确保功能性线粒体网络。受损的线粒体被称为线粒体自噬或线粒体自噬的过程降解,其中细胞器被自噬体吞噬,随后被递送到溶酶体进行降解。有证据表明,线粒体自噬对于细胞内稳态是重要的,并且减少的线粒体自噬导致功能障碍的线粒体的去除不足。在这篇综述中,我们讨论了线粒体自噬的调节和线粒体自噬的心脏保护作用的新证据。我们还讨论了靶向线粒体自噬治疗心血管疾病的前景。
Cardiac mitochondria are responsible for generating energy in the form of ATP through oxidative phosphorylation and are crucial for cardiac function. Mitochondrial dysfunction is a major contributor to loss of myocytes and development of heart failure. Myocytes have quality control mechanisms in place to ensure a network of functional mitochondria. Damaged mitochondria are degraded by a process called mitochondrial autophagy, or mitophagy, where the organelle is engulfed by an autophagosome and subsequently delivered to a lysosome for degradation. Evidence suggests that mitophagy is important for cellular homeostasis, and reduced mitophagy leads to inadequate removal of dysfunctional mitochondria. In this review, we discuss the regulation of mitophagy and the emerging evidence of the cardioprotective role of mitophagy. We also address the prospect of therapeutically targeting mitophagy to treat patients with cardiovascular disease.
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