Heart failure (HF) has a multifaceted and complex pathophysiology. Beyond neurohormonal, renin-angiotensin-aldosterone system, and adrenergic hyperactivation, a role for other pathophysiological determinants is emerging. Genetic and epigenetic factors are involved in this syndrome. In many maladaptive processes, the role of microRNAs (miRNAs) has been recently demonstrated. MiRNAs are small endogenous non-coding molecules of RNA involved in gene expression regulation, and they play a pivotal role in intercellular communication, being involved in different biological and pathophysiological processes. MiRNAs can modulate infarct area size, cardiomyocytes restoration, collagen deposition, and macrophage polarization. MiRNAs may be considered as specific biomarkers of hypertrophy and fibrosis. MiRNAs have been proposed as a therapeutical tool because their administration can contrast with myocardial pathophysiological remodeling leading to HF. Antimir and miRNA mimics are small oligonucleotides which may be administered in several manners and may be able to regulate the expression of specific and circulating miRNAs. Studies on animal models and on healthy humans demonstrate that these molecules are well tolerated and effective, opening the possibility of a therapeutic use of miRNAs in cases of HF. The application of miRNAs for diagnosis, prognostic stratification, and therapy fits in with the new concept of a personalized and tailored approach to HF.
Keywords: biomarkers; diagnosis; fibrosis; heart failure; hypertrophy; miRNAs; therapy.