Calpain: the regulatory point of myocardial ischemia-reperfusion injury

Guo-Yang Liu; Wan-Li Xie; Yan-Ting Wang; Lu Chen; Zhen-Zhen Xu; Yong Lv; Qing-Ping Wu

doi:10.3389/fcvm.2023.1194402

Calpain: the regulatory point of myocardial ischemia-reperfusion injury

Front Cardiovasc Med. 2023 Jun 29:10:1194402. doi: 10.3389/fcvm.2023.1194402. eCollection 2023.

Authors

Guo-Yang Liu^#^{1

2

3}, Wan-Li Xie^#^{1

2

3}, Yan-Ting Wang^{1

2

3}, Lu Chen^{1

2

3}, Zhen-Zhen Xu^{1

2

3}, Yong Lv^{1

2

3}, Qing-Ping Wu^{1

2

3}

Affiliations

¹ Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
² Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
³ Key Laboratory of Anesthesiology and Resuscitation (Huazhong University of Science and Technology), Ministry of Education, Wuhan, China.

^# Contributed equally.

Abstract

Calpain is a conserved cysteine protease readily expressed in several mammalian tissues, which is usually activated by Ca²⁺ and with maximum activity at neutral pH. The activity of calpain is tightly regulated because its aberrant activation will nonspecifically cleave various proteins in cells. Abnormally elevation of Ca²⁺ promotes the abnormal activation of calpain during myocardial ischemia-reperfusion, resulting in myocardial injury and cardiac dysfunction. In this paper, we mainly reviewed the effects of calpain in various programmed cell death (such as apoptosis, mitochondrial-mediated necrosis, autophagy-dependent cell death, and parthanatos) in myocardial ischemia-reperfusion. In addition, we also discussed the abnormal activation of calpain during myocardial ischemia-reperfusion, the effect of calpain on myocardial repair, and the possible future research directions of calpain.

Keywords: apoptosis; calpain; myocardial ischemia-reperfusion injury; parthanatos; programmed cell death.

Publication types

Review

Grants and funding

This work was supported by the National Natural Science Foundation of China (Grant No. 81873952), the National Key Research and Development Program of China (Grant No. 2018YFC2001903), and the National Natural Science Foundation of China (Grant No. 81901948).