The pathophysiological role of MiRNAs in heart failure

Heart failure (HF) is a growing global health issue, chiefly marked by inexorable myocyte loss, maladaptive remodeling, and energetic failure. MicroRNAs (miRNAs) function as the principal post-transcriptional regulators of gene networks capable of facilitating the pathophysiology of illnesses. However, there is limited systemic-level understanding of their participation in human HF. Therefore, the miRNA mechanisms that modulate apoptosis, autophagy, myocardial fibrosis, inflammatory response, and energy metabolism of cardiomyocytes to inhibit and treat HF are elucidated in this work.

A analysis of the mechanisms utilized by miRNAs in the modulation of HF was performed following the retrieval of literature on the mechanism of action of miRNAs in HF. The literature was obtained from PubMed and Web of Science databases between 2021 and 2025.

The multi-dimensional regulatory function of miRNAs in HF was uncovered. At the cellular fate level, they mediate the survival and death of the myocardium and inhibit excessive apoptosis and oxidative damage. At the organizational structure level, they inhibit the advancement of pathological ventricular remodeling and fibrosis. At the energy homeostasis level, they control autophagy and energy metabolism of cells. Finally, at the inflammatory and signaling levels, they suppress the inflammatory storm and maintain calcium signaling homeostasis. A sophisticated and dynamic regulatory system consisting of various miRNAs was observed, which offers a theoretical basis and potential targets for HF mechanism research and targeted intervention.

MicroRNAs (miRNAs) jointly affect the survival, remodeling and energy balance of cardiac muscle cells. However, the clinical application of miRNAs in HF is still in the early exploration stage, and their true diagnostic value and therapeutic potential need to be further confirmed by rigorous and large-scale clinical studies.