Trim72, also known as MG53, is a member of the tripartite motif protein family and functions as an E3 ubiquitin ligase. It plays a crucial role in membrane repair, anti-inflammatory processes, and is involved in multiple signaling pathways such as FAK/Akt, STAT3/Notch-1, and PI3K-AKT [1,3,4]. It has significant biological importance in various physiological and pathological processes across multiple organs [1]. Genetic models, like gene knockout (KO) mouse models, have been valuable in studying Trim72's functions.

In Trim72 knockout mice, increased mortality, organ fungal burden, and kidney damage were observed after lethal Candida albicans infection, indicating its positive regulation of antifungal immunity [2]. In mdx mice (a model for Duchenne muscular dystrophy), decreased Trim72 expression was found in skeletal muscles, and overexpressing Trim72 via AAV-TRIM72 alleviated muscle inflammation by promoting mitophagy-mediated NLRP3 inflammasome inactivation [5]. In the context of colorectal cancer, lower Trim72 levels in liver metastases compared to primary tumors were associated with lymph node metastasis and advanced clinical stages, and Trim72 overexpression inhibited cell migration and epithelial-mesenchymal transition, while knockout increased these processes [3].

In conclusion, Trim72 has diverse essential biological functions including membrane repair, anti-inflammatory effects, and regulation of cell migration and immunity. KO mouse models have revealed its significance in diseases such as fungal infections, Duchenne muscular dystrophy, and colorectal cancer, providing valuable insights into disease mechanisms and potential therapeutic targets.