Lin Kai-Lieh, Chen Shang-Der, Lin Kai-Jung, Liou Chia-Wei, Chuang Yao-Chung, Wang Pei-Wen, Chuang Jiin-Haur, Lin Tsu-Kung
Center for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Department of Anesthesiology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Front Cell Dev Biol. 2021 Mar 22;9:636295. doi: 10.3389/fcell.2021.636295. eCollection 2021.
Cardiovascular diseases are one of the leading causes of death and global health problems worldwide. Multiple factors are known to affect the cardiovascular system from lifestyles, genes, underlying comorbidities, and age. Requiring high workload, metabolism of the heart is largely dependent on continuous power supply via mitochondria through effective oxidative respiration. Mitochondria not only serve as cellular power plants, but are also involved in many critical cellular processes, including the generation of intracellular reactive oxygen species (ROS) and regulating cellular survival. To cope with environmental stress, mitochondrial function has been suggested to be essential during bioenergetics adaptation resulting in cardiac pathological remodeling. Thus, mitochondrial dysfunction has been advocated in various aspects of cardiovascular pathology including the response to ischemia/reperfusion (I/R) injury, hypertension (HTN), and cardiovascular complications related to type 2 diabetes mellitus (DM). Therefore, mitochondrial homeostasis through mitochondrial dynamics and quality control is pivotal in the maintenance of cardiac health. Impairment of the segregation of damaged components and degradation of unhealthy mitochondria through autophagic mechanisms may play a crucial role in the pathogenesis of various cardiac disorders. This article provides in-depth understanding of the current literature regarding mitochondrial remodeling and dynamics in cardiovascular diseases.
心血管疾病是全球范围内主要的死亡原因和全球性健康问题之一。已知多种因素会从生活方式、基因、潜在合并症和年龄等方面影响心血管系统。心脏工作负荷大,其代谢很大程度上依赖于线粒体通过有效的氧化呼吸持续提供能量。线粒体不仅是细胞的能量工厂,还参与许多关键的细胞过程,包括细胞内活性氧(ROS)的产生和调节细胞存活。为应对环境压力,线粒体功能被认为在生物能量适应过程中至关重要,而这会导致心脏病理重塑。因此,线粒体功能障碍在心血管病理学的各个方面都有涉及,包括对缺血/再灌注(I/R)损伤、高血压(HTN)以及与2型糖尿病(DM)相关的心血管并发症的反应。所以,通过线粒体动力学和质量控制实现线粒体稳态对于维持心脏健康至关重要。通过自噬机制对受损成分进行隔离以及对不健康线粒体进行降解的功能受损,可能在各种心脏疾病的发病机制中起关键作用。本文深入介绍了当前有关心血管疾病中线粒体重塑和动力学的文献。