Trim72, also known as MG53, is a member of the tripartite motif protein family. It has multiple functions including a classic membrane repair function, anti-inflammatory ability, and E3 ubiquitin ligase properties. It participates in important physiological and pathological processes of multiple organs, and is involved in pathways such as NF-κB, ERK1/2, FAK/Akt, and PI3K-AKT [1,2,3].

In Trim72 knockout mouse models, 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), over-expressing Trim72 alleviates muscle inflammation by promoting mitophagy-mediated NLRP3 inflammasome inactivation [5]. In a cardiac hypertrophy model using transverse aortic constriction, in vivo silencing of Trim72 reversed TAC-induced cardiac fibrosis [4]. In colorectal cancer, overexpression of Trim72 inhibits cell migration and epithelial-mesenchymal transition, while knockout increases these processes [3].

In conclusion, Trim72 plays crucial roles in various biological processes and diseases. Gene knockout models in mice have revealed its significance in antifungal immunity, muscle inflammation, cardiac fibrosis, and cancer metastasis. These findings suggest Trim72 could be a potential therapeutic target for related diseases.

References:

1. Wang, Yong-Fei, An, Zi-Yi, Li, Jian-Wen, Dong, Zi-Kai, Jin, Wei-Lin. 2024. MG53/TRIM72: multi-organ repair protein and beyond. In Frontiers in physiology, 15, 1377025. doi:10.3389/fphys.2024.1377025. https://pubmed.ncbi.nlm.nih.gov/38681139/

2. Tan, Wang, Liu, Jiayu, Yu, Renlin, Lai, Xiaofei, Cao, Ju. 2024. Trim72 is a major host factor protecting against lethal Candida albicans infection. In PLoS pathogens, 20, e1012747. doi:10.1371/journal.ppat.1012747. https://pubmed.ncbi.nlm.nih.gov/39585917/

3. Faleti, Oluwasijibomi Damola, Gong, Yibing, Long, Jingyi, Yao, Jinke, Wu, Gongfa. 2024. TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer. In Heliyon, 10, e37714. doi:10.1016/j.heliyon.2024.e37714. https://pubmed.ncbi.nlm.nih.gov/39315132/

4. Chen, Xu, Su, Jie, Feng, Jianyu, Qiu, Chen, Zheng, Qijun. 2019. TRIM72 contributes to cardiac fibrosis via regulating STAT3/Notch-1 signaling. In Journal of cellular physiology, 234, 17749-17756. doi:10.1002/jcp.28400. https://pubmed.ncbi.nlm.nih.gov/30820965/

5. Wu, Mengli, Li, Huan, He, Juanjuan, Liu, Yanmei, Zhang, Weixi. 2023. TRIM72 Alleviates Muscle Inflammation in mdx Mice via Promoting Mitophagy-Mediated NLRP3 Inflammasome Inactivation. In Oxidative medicine and cellular longevity, 2023, 8408574. doi:10.1155/2023/8408574. https://pubmed.ncbi.nlm.nih.gov/36713032/