Elucidation of molecular bases for phenotypical modification of dilated cardiomyopathy by environmental factors

点击翻译按钮获取中文摘要

As animal models for dilated cardiomyopathy (DCM), we analyzed the knock-in mice in which a deletion of 3 base pairs coding for K210 in cardiac troponin (TNNT2) found in familial dilated cardiomyopathy (DCM) patients was introduced into endogenous genes. Although mice homozygous for TNNT2 mutant allele (TNNT2 delta210/delta210) exhibited progressive left ventricular chamber dilatation and systolic dysfunction and died due to heart failure, mice heterozygous for TNNT2 mutant allele (TNNT2 delta210/+) did not show the cardiomyopathic phenotype. In TNNT2 delta210/+ mice, the left ventricular systolic function and the arrythmogenicity of ventricular tachycardia/fibrillation were not influenced by high salt intake or high-fat and high-sucrose diet. These results suggest that dietary environment exerts marginal effects on cardiomyopathic phenotype in DCM model mice with the TNNT2 mutation.