Cardiac effects and clinical applications of MG53

Weina Zhong,Peter H U Lee,Chuanxi Cai,Jianjie Ma,Dathe Z Benissan-Messan

doi:10.1186/s13578-021-00629-x

Weina Zhong, Peter H U Lee + Show 3 more

Open Access

https://doi.org/10.1186/s13578-021-00629-x

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Abstract

Heart disease remains the leading cause of mortality globally, so further investigation is required to identify its underlying mechanisms and potential targets for treatment and prevention. Mitsugumin 53 (MG53), also known as TRIM72, is a TRIM family protein that was found to be involved in cell membrane repair and primarily found in striated muscle. Its role in skeletal muscle regeneration and myogenesis has been well documented. However, accumulating evidence suggests that MG53 has a potentially protective role in heart tissue, including in ischemia/reperfusion injury of the heart, cardiomyocyte membrane injury repair, and atrial fibrosis. This review summarizes the regulatory role of MG53 in cardiac tissues, current debates regarding MG53 in diabetes and diabetic cardiomyopathy, as well as highlights potential clinical applications of MG53 in treating cardiac pathologies.

Highlights

Mitsugumin-53 (MG53), known as TRIM72, is a cell membrane repair protein that is part of the tripartite motif family of proteins
We summarize the biological function of MG53 with its potential mechanisms in cardiac tissue (Fig. 1), discuss current debates regarding the role of MG53 in diabetic cardiomyopathy (Table 1), and potential clinical applications of recombinant MG53 protein in the management and treatment of heart diseases (Table 2)
Potential clinical applications Based on the known cardioprotective effects of MG53, recombinant human MG53 (rhMG53) protein could potentially be used as a therapeutic protein to prevent, attenuate, or treat cardiac tissue injury from myocardial infarction (MI) or ischemic heart disease

Summary

Introduction

Mitsugumin-53 (MG53), known as TRIM72, is a cell membrane repair protein that is part of the tripartite motif family of proteins. A recent study from Xiao’s group showed that MG53 is secreted from the mouse heart in response to IPC or oxidative stress, and that the released MG53 protects the heart against IR injury via increased phosphorylation of protein kinase-C-δ (PKCδ) (Fig. 1) [18]. Administration of recombinant MG53 proteins to simulate increased circulating MG53 significantly restored IPC function in MG53 KO mice and protected their hearts from IR injury, even without IPC [18].

Results

Conclusion