Mitochondrial dysfunction in vascular endothelial cells and its role in atherosclerosis

Kai Qu; Fang Yan; Xian Qin; Kun Zhang; Wen He; Mingqing Dong; Guicheng Wu

doi:10.3389/fphys.2022.1084604

Mitochondrial dysfunction in vascular endothelial cells and its role in atherosclerosis

Front Physiol. 2022 Dec 20:13:1084604. doi: 10.3389/fphys.2022.1084604. eCollection 2022.

Authors

Kai Qu^{1

2}, Fang Yan^{3

4}, Xian Qin^{1

2}, Kun Zhang^{1

2}, Wen He⁵, Mingqing Dong⁴, Guicheng Wu¹

Affiliations

¹ Clinical Research Center for Endocrinology and Metabolic Diseases, Chongqing University Three Gorges Hospital, Chongqing, China.
² College of Bioengineering Chongqing University, Chongqing, China.
³ Department of Geriatrics, Geriatric Diseases Institute of Chengdu, Chengdu Fifth People's Hospital, Chengdu, Sichuan, China.
⁴ Center for Medicine Research and Translation, Chengdu Fifth People's Hospital, Chengdu, Sichuan, China.
⁵ Department of Geriatrics, Clinical trial center, Chengdu Fifth People's Hospital, Chengdu, Sichuan, China.

Abstract

The mitochondria are essential organelles that generate large amounts of ATP via the electron transport chain (ECT). Mitochondrial dysfunction causes reactive oxygen species accumulation, energy stress, and cell death. Endothelial mitochondrial dysfunction is an important factor causing abnormal function of the endothelium, which plays a central role during atherosclerosis development. Atherosclerosis-related risk factors, including high glucose levels, hypertension, ischemia, hypoxia, and diabetes, promote mitochondrial dysfunction in endothelial cells. This review summarizes the physiological and pathophysiological roles of endothelial mitochondria in endothelial function and atherosclerosis.

Keywords: atherosclerosis; endothelial cells; mitochondrial ROS; mitochondrial dysfunction; mitophagy.

Publication types

Review