Abstract
Under natural conditions, injured cells can be repaired rapidly through inherent biological processes. However, in the case of diabetes, cardiovascular disease, muscular dystrophy, and other degenerative conditions, the natural repair process is impaired. Repair of injury to the cell membrane is an important aspect of physiology. Inadequate membrane repair function is implicated in the pathophysiology of many human disorders. Recent studies show that Mitsugumin 53 (MG53), a TRIM family protein, plays a key role in repairing cell membrane damage and facilitating tissue regeneration. Clarifying the role of MG53 and its molecular mechanism are important for the application of MG53 in regenerative medicine. In this review, we analyze current research dissecting MG53′s function in cell membrane repair and tissue regeneration, and highlight the development of recombinant human MG53 protein as a potential therapeutic agent to repair multiple-organ injuries.
Highlights
The cell membrane allows a complex communication and exchange between the inside of a cell and its extracellular environment
We have shown that mg53−/− mice display abnormal lung structure and function under basal conditions, a finding consistent with the observation that Mitsugumin 53 (MG53) is present in the alveolar epithelia, where ablation of the MG53 gene leads to defective alveolar structure in the mutant mice [6]
In their elegant research published in Diabetes [24], they were able to demonstrate a null impact of whole-body ablation of MG53 or sustained elevation on glucose handling and insulin signaling
Summary
The cell membrane allows a complex communication and exchange between the inside of a cell and its extracellular environment. Based on the phylogenic tree, MG53 proteins are divided into two categories according to the variants of amino acids in different domains, such as RING finger, B-box zinc, and SPRY domain (Figure 1B and Table 2). Based on their functional domains, MG53 homology can be grouped into two categories. C242 is a critical cysteine residue involves in redox-dependent oligomerization of MG53 associated with cell membrane repair. Critical residue involves in redox-dependent oligomerization of MG53 sociated with celland membrane repair. C242 is critical cysteine residue involves in redox-dependent oligomerization of associatedC242 withiscell membrane repair.
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