Trim72, also named MG53, is a member of the tripartite motif protein family with E3 ubiquitin ligase properties. It is crucial for membrane repair, participating in anti-inflammatory processes and various signaling pathways such as PI3K-AKT, ERK, and NF-κB. Its functions have broad biological importance in multiple organ systems and disease contexts [1,3,4,7].

In Trim72 knockout mouse models, it has been shown that Trim72 deficiency significantly increases mortality, organ fungal burden, and kidney damage in mice after lethal Candida albicans infection, indicating its positive regulation of antifungal immunity [2]. In mdx mice (a model for Duchenne muscular dystrophy), the decreased expression of Trim72 is associated with increased NLRP3 inflammasome and impaired mitophagy, while over-expression of Trim72 alleviates muscle inflammation by promoting mitophagy-mediated NLRP3 inflammasome inactivation [6]. In the context of cardiac fibrosis, in vivo silencing of Trim72 reversed transverse aortic constriction (TAC)-induced cardiac fibrosis, highlighting its role in maintaining fibroblast-to-myofibroblast transition [5].

In conclusion, Trim72 plays essential roles in membrane repair, antifungal immunity, muscle inflammation regulation, and cardiac fibrosis through its involvement in various signaling pathways. The use of Trim72 knockout mouse models has provided valuable insights into its functions in these disease-related biological processes, suggesting its potential as a therapeutic target for treating conditions like fungal infections, muscular dystrophy, and cardiac fibrosis.