The main findings of this study are as follows: 1) DSELD protects H9C2 cells from CM-induced injuries; 2) DSELD restores the cardiac functions and reverses the pathological damages in a mouse model of myocardial hypertrophy; 3) DSELD modulates the levels of multiple inflammatory cytokines; 4) DSELD inhibits inflammation by downregulating the expression of inflammatory proteins such as MyD88 and MMP9, key components of the TLR4 signaling pathway. The gene discussed is PROS1; the disease is cardiac hypertrophy.