Tnni3-Cre Mouse

Troponin I (TnI), along with Troponin T (TnT) and Troponin C (TnC), forms the troponin complex in striated muscle. TnI, the inhibitory subunit, blocks actin-myosin interactions, facilitating muscle relaxation and providing a calcium-sensitive switch for muscle contraction. The TnI subfamily includes three genes, with TNNI3 encoding cardiac-specific TnI, expressed only in heart muscle ^[1]. Mutations in TNNI3 cause familial hypertrophic cardiomyopathy type 7 (CMH7) and restrictive cardiomyopathy (RCM). TnI helps diagnose heart failure and ischemic heart disease, and elevated troponin levels indicate acute myocardial injury in moderate/severe COVID-19 patients. In COVID-19-related cardiovascular diseases, elevated troponin correlates with higher mortality risk.

Tnni3-Cre mice were constructed by integrating the Cre-rBG pA gene expression component into the mouse Tnni3 gene by gene editing, a strategy that disrupts the expression of the endogenous Tnni3 gene in mice. When Tnni3-Cre mice are crossed with mice containing loxP sites, sequence recombination mediated by Cre recombinase occurs in the offspring's cardiomyocytes.