Furthermore, it exerted a protective effect in sepsis: MIR503HG overexpression could effectively alleviate SICD and mitigate the inflammatory response, as evidenced by decreased left ventricular end-diastolic pressure, increased left ventricular systolic pressure, reduced levels of CK-MB and cTnI, as well as restored myocardial systolic/diastolic capacity (maximal rate of left ventricular pressure rise/fall [±dP/dt]). Here, TNNI3 is linked to Sepsis.