Molecular pathogenesis of heart failure in diabetes mellitus – new direction for the therapeutic approach

Abstract

As it has been proven, cardiovascular diseases are several times more common in diabetic patients than in the general population. Despite many studies and hypotheses, is still not explained why this happens. Considering the frequent coexistence of cardiovascular risk factors with diabetes, the identification of diabetic cardiomyopathy as an independent complication is controversial, and diagnosis in clinical practice is rare. Nevertheless, the presence of diabetes significantly worsens the course and prognosis of cardiovascular diseases, and a better understanding of the diabetic component in the development of heart failure seems essential in the search for an effective therapy. The pathogenetic factors of the development of heart failure in diabetes include: metabolic disorders related to hyperglycaemia, lipotoxicity, insulin resistance, oxidative stress, immune system dysfunction, genetic predisposition and epigenetic disorders. The clinical pictures of diabetic cardiomyopathy vary depending on the type of diabetes, and dysfunction includes not only the cells of the myocardium, as well as stromal cells, endothelial and nervous system cells. The long-term and asymptomatic course of this complication and its progressive nature shortening the lives of diabetic patients prompt the search for new diagnostic and therapeutic methods. A better understanding of the molecular basis of myocardial dysfunction in diabetes appears essential in the search. Stopping the “cascade” of pathways responsible for activation of inflammation, fibrosis or apoptosis in individual organs could effectively prevent the development of diabetic complications. The paper presents existing pathogenetic concepts and their therapeutic implications, which may be used in the prevention of cardiovascular complications in diabetes and allow individualization of therapy.