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Assessment of mitochondrial dysfunction and implications in cardiovascular disorders

Li, Yuan; Ma, Ying; Dang, Qing Ya; Fan, Xin Rong; Han, Chu Ting; Xu, Shang Zhong; Li, Peng Yun

Authors

Yuan Li

Ying Ma

Qing Ya Dang

Xin Rong Fan

Chu Ting Han

Peng Yun Li



Abstract

Mitochondria play a pivotal role in cellular function, not only acting as the powerhouse of the cell, but also regulating ATP synthesis, reactive oxygen species (ROS) production, intracellular Ca2+ cycling, and apoptosis. During the past decade, extensive progress has been made in the technology to assess mitochondrial functions and accumulating evidences have shown that mitochondrial dysfunction is a key pathophysiological mechanism for many diseases including cardiovascular disorders, such as ischemic heart disease, cardiomyopathy, hypertension, atherosclerosis, and hemorrhagic shock. The advances in methodology have been accelerating our understanding of mitochondrial molecular structure and function, biogenesis and ROS and energy production, which facilitates new drug target identification and therapeutic strategy development for mitochondrial dysfunction-related disorders. This review will focus on the assessment of methodologies currently used for mitochondrial research and discuss their advantages, limitations and the implications of mitochondrial dysfunction in cardiovascular disorders.

Citation

Li, Y., Ma, Y., Dang, Q. Y., Fan, X. R., Han, C. T., Xu, S. Z., & Li, P. Y. (2022). Assessment of mitochondrial dysfunction and implications in cardiovascular disorders. Life Sciences, 306, Article 120834. https://doi.org/10.1016/j.lfs.2022.120834

Journal Article Type Review
Acceptance Date Jul 20, 2022
Online Publication Date Jul 25, 2022
Publication Date Oct 1, 2022
Deposit Date Aug 30, 2022
Publicly Available Date Jan 31, 2024
Journal Life Sciences
Print ISSN 0024-3205
Publisher Elsevier
Peer Reviewed Peer Reviewed
Volume 306
Article Number 120834
DOI https://doi.org/10.1016/j.lfs.2022.120834
Keywords Mitochondrial dysfunction; Mitochondrial dynamics; Oxidative stress; Mitochondrial energy metabolism; Ca2+ signaling; Mitochondrial permeability transition pore
Public URL https://hull-repository.worktribe.com/output/4063165

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