Gastrodin regulates H3K14la through the CDT2-KAT2A axis to treat Sepsis-induced myocardial dysfunction

In this study, we demonstrated that GAS exerts a protective effect against SIMD by enhancing the binding of CDT2 to KAT2A, affecting the stability of KAT2A, and regulating H3K14la, thereby remodeling energy metabolism. This finding offers significant insights and potential targets for the development of novel therapeutic agents for SIMD in the future. Moreover, it provides new evidence for the subsequent screening and investigation of the mechanisms underlying the treatment of SIMD.