Mitochondrial Quality Control in the Heart: The Balance between Physiological and Pathological Stress

被引:12
|
作者
Fajardo, Giovanni [1 ,2 ]
Coronado, Michael [3 ]
Matthews, Melia [4 ]
Bernstein, Daniel [1 ,2 ]
机构
[1] Stanford Univ, Dept Pediat, Stanford, CA 94305 USA
[2] Stanford Univ, Cardiovasc Inst, Stanford, CA 94305 USA
[3] Cytokinet Inc, San Francisco, CA 94080 USA
[4] Cornell Univ, Dept Biomed & Biol Sci, Ithaca, NY 14850 USA
基金
美国国家卫生研究院;
关键词
mitochondria; fission; fusion; mitophagy; biogenesis; ISCHEMIA/REPERFUSION INJURY; ACTIVE MITOCHONDRIA; CELL-DEATH; MITOPHAGY; FISSION; AUTOPHAGY; DYSFUNCTION; DYNAMICS; FUSION; DRP1;
D O I
10.3390/biomedicines10061375
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alterations in mitochondrial function and morphology are critical adaptations to cardiovascular stress, working in concert in an attempt to restore organelle-level and cellular-level homeostasis. Processes that alter mitochondrial morphology include fission, fusion, mitophagy, and biogenesis, and these interact to maintain mitochondrial quality control. Not all cardiovascular stress is pathologic (e.g., ischemia, pressure overload, cardiotoxins), despite a wealth of studies to this effect. Physiological stress, such as that induced by aerobic exercise, can induce morphologic adaptations that share many common pathways with pathological stress, but in this case result in improved mitochondrial health. Developing a better understanding of the mechanisms underlying alterations in mitochondrial quality control under diverse cardiovascular stressors will aid in the development of pharmacologic interventions aimed at restoring cellular homeostasis.
引用
收藏
页数:14
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