Dilated cardiomyopathy: from genes and molecules to potential treatments.

Abstract

Dilated cardiomyopathy is a myocardial condition marked by the enlargement of the heart's ventricular chambers and the gradual decline in systolic function, frequently resulting in congestive heart failure. Dilated cardiomyopathy has obvious familial characteristics, and mutations in related pathogenic genes can account for about 50% of patients with dilated cardiomyopathy. The most common genes related to dilated cardiomyopathy include TTN, LMNA, MYH7, etc. With more and more research on these genes, it will undoubtedly provide more potential targets and therapeutic pathways for the treatment of dilated cardiomyopathy. In addition, myocardial inflammation, myocardial metabolism abnormalities and cardiomyocyte apoptosis all have an important impact on the pathogenesis of dilated cardiomyopathy. Approximately half of sudden deaths among children and adolescents, along with the majority of patients undergoing heart transplantation, stem from cardiomyopathy. Therefore, precise and prompt clinical diagnosis holds paramount importance. Currently, diagnosis primarily hinges on the patient's medical background and imaging tests, with the significance of genetic testing steadily gaining prominence. The primary treatment for dilated cardiomyopathy remains heart transplantation. However, the scarcity of donors and the risk of severe immune rejection underscore the pressing need for novel therapies. Presently, research is actively exploring preclinical treatments like stem cell therapy as potential solutions.