Fajardo Giovanni, Coronado Michael, Matthews Melia, Bernstein Daniel
Department of Pediatrics and the Cardiovascular Institute, Stanford University, Stanford, CA 94305, USA.
Cytokinetics Inc., South San Francisco, CA 94080, USA.
Biomedicines. 2022 Jun 10;10(6):1375. doi: 10.3390/biomedicines10061375.
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.
线粒体功能和形态的改变是对心血管应激的关键适应性反应,它们协同作用以恢复细胞器水平和细胞水平的稳态。改变线粒体形态的过程包括裂变、融合、线粒体自噬和生物发生,这些过程相互作用以维持线粒体质量控制。尽管有大量关于此的研究,但并非所有心血管应激都是病理性的(例如,缺血、压力过载、心脏毒素)。生理应激,如有氧运动诱导的应激,可诱导与病理应激有许多共同途径的形态学适应,但在这种情况下会改善线粒体健康。更好地理解不同心血管应激源下线粒体质量控制改变的潜在机制,将有助于开发旨在恢复细胞稳态的药物干预措施。