Pohjoismäki Jaakko L, Goffart Steffi
University of Eastern Finland, Department of Environmental and Biological Sciences, P.O. Box 111, 80101 Joensuu, Finland.
University of Eastern Finland, Department of Environmental and Biological Sciences, P.O. Box 111, 80101 Joensuu, Finland.
Free Radic Biol Med. 2017 May;106:345-354. doi: 10.1016/j.freeradbiomed.2017.02.032. Epub 2017 Feb 17.
Mitochondria are essential for the development as well as maintenance of the myocardium, the most energy consuming tissue in the human body. Mitochondria are not only a source of ATP energy but also generators of reactive oxygen species (ROS), that cause oxidative damage, but also regulate physiological processes such as the switch from hyperplastic to hypertrophic growth after birth. As excess ROS production and oxidative damage are associated with cardiac pathology, it is not surprising that much of the research focused on the deleterious aspects of free radicals. However, cardiomyocytes are naturally highly adapted against repeating oxidative insults, with evidence suggesting that moderate and acute ROS exposure has beneficial consequences for mitochondrial maintenance and cardiac health. Antioxidant defenses, mitochondrial quality control, mtDNA maintenance mechanisms as well as mitochondrial fusion and fission improve mitochondrial function and cardiomyocyte survival under stress conditions. As these adaptive processes can be induced, promoting mitohormesis or mitochondrial biogenesis using controlled ROS exposure could provide a promising strategy to increase cardiomyocyte survival and prevent pathological remodeling of the myocardium.
线粒体对于心肌的发育和维持至关重要，心肌是人体中能量消耗最大的组织。线粒体不仅是ATP能量的来源，也是活性氧（ROS）的产生者，ROS会导致氧化损伤，但也调节生理过程，如出生后从增生性生长向肥厚性生长的转变。由于过量的ROS产生和氧化损伤与心脏病理相关，因此许多研究聚焦于自由基的有害方面也就不足为奇了。然而，心肌细胞天生对反复的氧化损伤具有高度适应性，有证据表明适度和急性的ROS暴露对线粒体维持和心脏健康有有益影响。抗氧化防御、线粒体质量控制、线粒体DNA维持机制以及线粒体融合和裂变可在应激条件下改善线粒体功能和心肌细胞存活。由于这些适应性过程可以被诱导，使用可控的ROS暴露来促进线粒体应激反应或线粒体生物发生可能为提高心肌细胞存活和预防心肌病理重塑提供一种有前景的策略。
