Corin is regulated by miR-19b-1-5p to inhibit Ang II-induced atrial fibrillation.

Abstract

BACKGROUND: Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia globally, leading to increased mortality and morbidity. Corin has been shown to play an important role in AF in clinical trials, but the specific mechanism is unknown. OBJECTIVE: This study aimed to investigate the molecular mechanisms underlying AF by examining the roles of Corin protein and miR-19b-1-5p in AF pathogenesis. METHODS: The study used an angiotensin II (Ang II)-induced AF mouse model to assess the impact of Corin and miR-19b-1-5p on atrial remodeling. Various techniques including molecular analysis, histological staining, and gene expression profiling were employed to evaluate the effects of Corin and miR-19b-1-5p in the development of AF. RESULTS: The research demonstrated that knockdown of Corin exacerbated Ang II-induced atrial electrical and structural remodeling, contributing to atrial fibrosis and AF progression. Knockdown of Corin exacerbated atrial electrical and structural remodeling induced by Ang II, resulting in increased atrial size, elevated AF incidence, enhanced fibrosis, and oxidative stress levels. Furthermore, miR-19b-1-5p was identified as a negative regulator of Corin messenger ribonucleic acid expression, influencing atrial remodeling in the Ang II-induced AF model. CONCLUSION: The findings suggest that both miR-19b-1-5p and Corin offer valuable insights into the molecular mechanisms of AF. Targeting these molecules may present potential therapeutic strategies for the treatment of AF in the future.