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通过氧消耗率评估心肌细胞中的线粒体功能障碍和毒性。

Oxygen consumption rate to evaluate mitochondrial dysfunction and toxicity in cardiomyocytes.

作者信息

Ahn Dohee, Go Ryeo-Eun, Choi Kyung-Chul

机构信息

Laboratory of Biochemistry and Immunology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644 Republic of Korea.

出版信息

Toxicol Res. 2023 Jun 13;39(3):333-339. doi: 10.1007/s43188-023-00183-3. eCollection 2023 Jul.

DOI:10.1007/s43188-023-00183-3
PMID:37398565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10313613/
Abstract

The increase in the types and complexity of diseases has led to significant advances in diagnostic techniques and the availability of effective therapies. Recent studies have focused on the role of mitochondrial dysfunction in the pathogenesis of cardiovascular diseases (CVDs). Mitochondria are important organelles in cells that generate energy. Besides the production of adenosine triphosphate (ATP), the energy currency of cells, mitochondria are also involved in thermogenesis, control of intracellular calcium ions (Ca), apoptosis, regulation of reactive oxygen species (ROS), and inflammation. Mitochondrial dysfunction has been implicated in several diseases including cancer, diabetes, some genetic diseases, and neurogenerative and metabolic diseases. Furthermore, the cardiomyocytes of the heart are rich in mitochondria due to the large energy requirement for optimal cardiac function. One of the main causes of cardiac tissue injuries is believed to be mitochondrial dysfunction, which occurs via complicated pathways which have not yet been completely elucidated. There are various types of mitochondrial dysfunction including mitochondrial morphological change, unbalanced levels of substances to maintain mitochondria, mitochondrial damage by drugs, and mitochondrial deletion and synthesis errors. Most of mitochondrial dysfunctions are linked with symptoms and diseases, thus we focus on parts of mitochondrial dysfunction about fission and fusion in cardiomyocytes, and ways to understand the mechanism of cardiomyocyte damage by detecting oxygen consumption levels in the mitochondria.

摘要

疾病类型和复杂性的增加推动了诊断技术的显著进步以及有效治疗方法的出现。最近的研究聚焦于线粒体功能障碍在心血管疾病(CVDs)发病机制中的作用。线粒体是细胞中产生能量的重要细胞器。除了产生细胞的能量货币三磷酸腺苷(ATP)外,线粒体还参与产热、细胞内钙离子(Ca)的控制、细胞凋亡、活性氧(ROS)的调节以及炎症反应。线粒体功能障碍与多种疾病有关,包括癌症、糖尿病、一些遗传疾病以及神经退行性和代谢性疾病。此外,由于心脏最佳功能对能量的大量需求,心脏的心肌细胞富含线粒体。心脏组织损伤的主要原因之一被认为是线粒体功能障碍,其通过尚未完全阐明的复杂途径发生。线粒体功能障碍有多种类型,包括线粒体形态变化、维持线粒体的物质水平失衡、药物对线粒体的损伤以及线粒体缺失和合成错误。大多数线粒体功能障碍与症状和疾病相关,因此我们关注心肌细胞中线粒体分裂和融合方面的部分功能障碍,以及通过检测线粒体中的氧消耗水平来理解心肌细胞损伤机制的方法。

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RhoA rescues cardiac senescence by regulating Parkin-mediated mitophagy.RhoA 通过调节 Parkin 介导的线粒体自噬来挽救心脏衰老。
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Klf4 deficiency exacerbates myocardial ischemia/reperfusion injury in mice via enhancing ROCK1/DRP1 pathway-dependent mitochondrial fission.Klf4基因缺失通过增强ROCK1/DRP1途径依赖性线粒体分裂加重小鼠心肌缺血/再灌注损伤。
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