Theranostics 2021; 11(14):6766-6785. doi:10.7150/thno.60143 This issue


Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control

Xing Chang1,2, Amanda Lochner3, Hsueh-Hsiao Wang4, Shuyi Wang5,6, Hang Zhu1, Jun Ren5, Hao Zhou1,5✉

1. Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing 100853, China.
2. Guang'anmen Hospital of Chinese Academy of Traditional Chinese Medicine, Beijing, China.
3. Department of Biomedical Sciences, Faculty of Health Sciences, University of Stellenbosch, Stellenbosch, South Africa.
4. Department of Medicine, Mackay Medical College, New Taipei City, 252, Taiwan.
5. University of Wyoming College of Health Sciences, Laramie, WY 82071, USA.
6. Shanghai University School of Medicine, Shanghai 200044, China.

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Chang X, Lochner A, Wang HH, Wang S, Zhu H, Ren J, Zhou H. Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control. Theranostics 2021; 11(14):6766-6785. doi:10.7150/thno.60143. Available from

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Graphic abstract

Endothelial cells (ECs) constitute the innermost layer in all blood vessels to maintain the structural integrity and microcirculation function for coronary microvasculature. Impaired endothelial function is demonstrated in various cardiovascular diseases including myocardial infarction (MI), which is featured by reduced myocardial blood flow as a result of epicardial coronary obstruction, thrombogenesis, and inflammation. In this context, understanding the cellular and molecular mechanisms governing the function of coronary ECs is essential for the early diagnosis and optimal treatment of MI. Although ECs contain relatively fewer mitochondria compared with cardiomyocytes, they function as key sensors of environmental and cellular stress, in the regulation of EC viability, structural integrity and function. Mitochondrial quality control (MQC) machineries respond to a broad array of stress stimuli to regulate fission, fusion, mitophagy and biogenesis in mitochondria. Impaired MQC is a cardinal feature of EC injury and dysfunction. Hence, medications modulating MQC mechanisms are considered as promising novel therapeutic options in MI. Here in this review, we provide updated insights into the key role of MQC mechanisms in coronary ECs and microvascular dysfunction in MI. We also discussed the option of MQC as a novel therapeutic target to delay, reverse or repair coronary microvascular damage in MI. Contemporary available MQC-targeted therapies with potential clinical benefits to alleviate coronary microvascular injury during MI are also summarized.

Keywords: coronary microvasculature, ECs, myocardial infarction, mitochondrial quality control