a Department of Neurochemistry, Division of Basic and Applied Neurobiology , Serbsky Federal Medical Research Center of Psychiatry and Narcology , Moscow , Russia.
b Department of Genetics, Southern Federal University , Rostov-on-Don , Russia.
Ann Med. 2018 Mar;50(2):121-127. doi: 10.1080/07853890.2017.1417631. Epub 2017 Dec 18.
Cardiovascular disease (CVD) is a leading cause of mortality worldwide. Proper mitochondrial function is necessary in tissues and organs that are of high energy demand, including the heart. Mitochondria are very sensitive to nutrient and oxygen supply and undergo metabolic adaptation to the changing environment. In CVD, such an adaptation is impaired, which, in turn, leads to a progressive decline of the mitochondrial function associated with abnormalities in the respiratory chain and ATP synthesis, increased oxidative stress, and loss of the structural integrity of mitochondria. Uncoupling of the electron transport chain in dysfunctional mitochondria results in enhanced production of reactive oxygen species, depletion of cell ATP pool, extensive cell damage, and apoptosis of cardiomyocytes. Mitophagy is a process, during which cells clear themselves from dysfunctional and damaged mitochondria using autophagic mechanism. Deregulation of this process in the failing heart, accumulation of dysfunctional mitochondria makes the situation even more adverse. In cardiac pathology, aberrations of the activity of the respiratory chain and ATP production may be considered as a core of mitochondrial dysfunction. Indeed, therapeutic restoration of these key functional properties can be considered as a primary goal for improvement of mitochondrial dysfunction in CVD. Key messages Mitochondrial dysfunction plays a crucial role in cardiovascular disease pathogenesis. Cardiovascular disease is associated with altered mithochondrial biogenesis and clearance. In cardiovascular disease, impaired mitochondrial function results in decreased ATP production and enhanced ROS formation.
心血管疾病（CVD）是全球范围内主要的死亡原因。在包括心脏在内的高能量需求组织和器官中，适当的线粒体功能是必需的。线粒体对营养和氧气供应非常敏感，并能适应不断变化的环境进行代谢适应。在 CVD 中，这种适应会受损，反过来又会导致与呼吸链和 ATP 合成异常、氧化应激增加以及线粒体结构完整性丧失相关的线粒体功能逐渐下降。功能失调的线粒体电子传递链解偶联会导致活性氧的产生增加、细胞 ATP 池耗竭、广泛的细胞损伤和心肌细胞凋亡。线粒体自噬是一种细胞利用自噬机制清除功能失调和受损线粒体的过程。衰竭心脏中该过程的失调会导致功能失调的线粒体积累，使情况更加恶化。在心脏病理学中，呼吸链活性和 ATP 产生的改变可以被认为是线粒体功能障碍的核心。事实上，恢复这些关键功能特性可以被认为是改善 CVD 中线粒体功能障碍的首要目标。要点 线粒体功能障碍在心血管疾病发病机制中起关键作用。 心血管疾病与改变的线粒体生物发生和清除有关。 在心血管疾病中，线粒体功能受损会导致 ATP 生成减少和 ROS 形成增加。
