Oxygen consumption rate to evaluate mitochondrial dysfunction and toxicity in cardiomyocytes

被引:3
|
作者
Ahn, Dohee [1 ]
Go, Ryeo-Eun [1 ]
Choi, Kyung-Chul [1 ]
机构
[1] Chungbuk Natl Univ, Coll Vet Med, Lab Biochem & Immunol, Cheongju 28644, Chungbuk, South Korea
基金
新加坡国家研究基金会;
关键词
Mitochondrial dysfunction; Oxygen consumption rate; Cardiomyocytes; Mitochondrial fission; KINASE INHIBITORS; AUTOPHAGY; HEART; PROTECTS; PINK1; BIOENERGETICS; MITOPHAGY; FISSION;
D O I
10.1007/s43188-023-00183-3
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
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 (Ca2+), 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.
引用
收藏
页码:333 / 339
页数:7
相关论文
共 50 条
  • [31] MITOCHONDRIAL OXYGEN CONSUMPTION AND PROTON VECTOR
    HATASE, O
    ODA, T
    JOURNAL OF BIOCHEMISTRY, 1971, 70 (04): : 549 - &
  • [32] Oxygen consumption by a bituminous coal: Time dependence of the rate of oxygen consumption
    Wang, HH
    Dlugogorski, BZ
    Kennedy, EM
    COMBUSTION SCIENCE AND TECHNOLOGY, 2002, 174 (09) : 147 - 167
  • [33] Mitochondrial dysfunction: Patient monitoring and toxicity management
    McComsey, G
    Lonergan, JT
    JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES, 2004, 37 : S30 - S35
  • [34] Role of mitochondrial dysfunction in cardiac glycoside toxicity
    Liu, Ting
    Brown, David A.
    O'Rourke, Brian
    JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2010, 49 (05) : 728 - 736
  • [35] ADAPTATION SPEED OF CARDIAC MITOCHONDRIAL OXYGEN-CONSUMPTION DECREASES WITH HIGHER HEART-RATE
    EIJGELSHOVEN, MHJ
    HAK, JB
    VANBEEK, JHGM
    WESTERHOF, N
    AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (06): : H1893 - H1898
  • [36] RESPONSE-TIME OF CARDIAC MITOCHONDRIAL OXYGEN-CONSUMPTION TO HEART-RATE STEPS
    VANBEEK, JHGM
    WESTERHOF, N
    AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (02): : H613 - H625
  • [37] EMBRYO OXYGEN CONSUMPTION TO EVALUATE THE EMBRYO QUALITY.
    Fukui, A.
    Takeyama, R.
    Wakimoto, Y.
    Ukita, Y.
    Shibahara, H.
    FERTILITY AND STERILITY, 2018, 110 (04) : E354 - E354
  • [38] Modeling drug-induced mitochondrial toxicity with human primary cardiomyocytes
    Xiaoli Tang
    Hong Liu
    Rongjia Rao
    Yafei Huang
    Mengqi Dong
    Miaomiao Xu
    Shanshan Feng
    Xun Shi
    Li Wang
    Zengwu Wang
    Bingying Zhou
    Science China(Life Sciences), 2024, 67 (02) : 301 - 319
  • [39] Protein kinase D activation induces mitochondrial fragmentation and dysfunction in cardiomyocytes
    Jhun, Bong Sook
    O-Uchi, Jin
    Adaniya, Stephanie M.
    Mancini, Thomas J.
    Cao, Jessica L.
    King, Michelle E.
    Landi, Amy K.
    Ma, Hanley
    Shin, Milla
    Yang, Donqin
    Xu, Xiaole
    Yoon, Yisang
    Choudhary, Gaurav
    Clements, Richard T.
    Mende, Ulrike
    Sheu, Shey-Shing
    JOURNAL OF PHYSIOLOGY-LONDON, 2018, 596 (05): : 827 - 855
  • [40] Modeling drug-induced mitochondrial toxicity with human primary cardiomyocytes
    Tang, Xiaoli
    Liu, Hong
    Rao, Rongjia
    Huang, Yafei
    Dong, Mengqi
    Xu, Miaomiao
    Feng, Shanshan
    Shi, Xun
    Wang, Li
    Wang, Zengwu
    Zhou, Bingying
    SCIENCE CHINA-LIFE SCIENCES, 2024, 67 (02) : 301 - 319