MG53 is a double-edged sword for human diseases.
Yan Zhang1, Hong-Kun Wu2, Feng-Xiang Lv2
1State Key Laboratory of Membrane Biology, Institute of Molecular Medicine, Peking University, Beijing 100871, China. zhangyan9876@pku.edu.cn.
Sheng Li Xue Bao : [Acta Physiologica Sinica]
|August 23, 2016
Summary
Mitsugumin 53 (MG53), a muscle protein, repairs cell membranes and protects organs from injury. However, it can also cause insulin resistance and metabolic diseases like type-2 diabetes.
Area of Science:
- Muscle protein biology
- Cellular repair mechanisms
- Metabolic disease pathways
Background:
- Mitsugumin 53 (MG53), also known as Trim72, is a TRIM-family protein highly expressed in cardiac and skeletal muscle.
- MG53 plays dual roles, acting as both a physiological protector and a pathogenic factor in various diseases.
Purpose of the Study:
- To comprehensively review the biological functions of MG53.
- To focus on MG53's clinical value as a therapeutic target for human diseases.
Main Methods:
- Literature review of MG53's physiological and pathogenic roles.
- Analysis of MG53's involvement in cell signaling pathways (PI3K-Akt-GSK3β, ERK1/2).
- Examination of MG53's function as an E3 ligase and its impact on insulin signaling.
Main Results:
- MG53 facilitates plasma membrane repair, preserving muscle integrity.
- MG53 mediates cardiac ischemic preconditioning/postconditioning via cell survival pathways.
- Systemic recombinant MG53 protects organs from injury; however, MG53's E3 ligase activity induces insulin resistance and metabolic diseases.
- MG53 negatively regulates myogenesis.
Conclusions:
- MG53's multifaceted roles require careful consideration for therapeutic strategies.
- Understanding MG53's functions is crucial for maximizing benefits and minimizing side effects in disease treatment.
