Trim35, a member of the tripartite motif (TRIM) family, functions as an E3 ubiquitin ligase. It is involved in multiple biological processes, including innate immune responses, cell growth, metabolism, and chromatin remodeling. It participates in pathways such as RIG-I-mediated antiviral immunity, cGAS-STING-mediated signaling, and mTORC1 activation, and is of great biological importance in the context of various diseases [1,3,4].

In Trim35-deficient mice, the production of type I interferon in response to viral infection was suppressed, making them more susceptible to influenza A virus infection, indicating its role in antiviral immunity [1]. Fibroblast-specific Trim35 gene knockout (Trim35cKO) mice showed improved cardiac fibrosis and hypertrophy, suggesting that TRIM35 in fibroblasts promotes cardiac remodeling through regulating SLC7A5-mediated amino acid transport and mTORC1 activation [3]. In cardiomyocyte-specific Trim35 overexpression transgenic mice, increased P53 transcriptional activity was observed, initiating heart failure, and these findings were recapitulated in human non-ischemic LV dilated cardiomyopathy samples [2].

In conclusion, Trim35 plays essential roles in innate immunity and multiple disease-related biological processes. Mouse models with Trim35 deficiency or overexpression have significantly contributed to understanding its role in viral infections, heart failure, and cardiac remodeling, providing potential therapeutic targets for related diseases.