MicroRNAs in Atrial Fibrillation: Mechanisms, Vascular Implications, and Therapeutic Potential

• Published in: Biomedicines Vol. 12; no. 4; p. 811
• Main Authors: Vardas, Emmanouil P, Theofilis, Panagiotis, Oikonomou, Evangelos, Vardas, Panos E, Tousoulis, Dimitris
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.04.2024
• Subjects: Antagonism; Arrhythmia; Atrial fibrillation; Cardiac arrhythmia; Cardiomyocytes; Collagen; Fibrillation; Fibroblasts; Fibrosis; Health aspects; Inflammation; Kinases; Mechanical properties; MicroRNA; MicroRNAs; miRNA; Oxidative stress; Pathophysiology; Physiology; Precision medicine; Public health; Quality of life; Thromboembolism; Tumor necrosis factor-TNF; Greece; microRNA; atrial fibrillation; fibrosis; inflammation; oxidative stress
• ISSN: 2227-9059; 2227-9059
• DOI: 10.3390/biomedicines12040811

Atrial fibrillation (AFib), the most prevalent arrhythmia in clinical practice, presents a growing global health concern, particularly with the aging population, as it is associated with devastating complications and an impaired quality of life. Its pathophysiology is multifactorial, including the pathways of fibrosis, inflammation, and oxidative stress. MicroRNAs (miRNAs), small non-coding RNA molecules, have emerged as substantial contributors in AFib pathophysiology, by affecting those pathways. In this review, we explore the intricate relationship between miRNAs and the aforementioned aspects of AFib, shedding light on the molecular pathways as well as the potential diagnostic applications. Recent evidence also suggests a possible role of miRNA therapeutics in maintenance of sinus rhythm via the antagonism of miR-1 and miR-328, or the pharmacological upregulation of miR-27b and miR-223-3p. Unraveling the crosstalk between specific miRNA profiles and genetic predispositions may pave the way for personalized therapeutic approaches, setting the tone for precision medicine in atrial fibrillation.