miR-92a as a potential biomarker and therapeutic target in heart failure: evidence from human and mouse studies.

Abstract

BACKGROUND: This research investigated the expression of microRNA-92a (miR-92a) in chronic heart failure (CHF) patients and assessed its regulatory mechanism using a transverse aortic constriction (TAC) mouse model. METHODS: Thirty patients with CHF (NYHA class II-IV) and 30 age and sex-matched healthy controls were enrolled from January 2021 to April 2022. Plasma levels of miR-92a were analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). In addition, we utilized the TAC heart failure mouse model (n&#x2009;=&#x2009;12) to evaluate the change in cardiac function following adeno-associated virus (AAV) mediated inhibition or overexpression of miR-92a. The following echocardiographic variables were evaluated: ejection fraction (EF), fractional shortening (FS), left ventricular internal diameter diastole (LVIDd), and left ventricular internal diameter systole (LVIDs). RESULTS: miR-92a levels were significantly increased in CHF patients and mice following tac application (p&#x2009;<&#x2009;0.01). Inhibition of miR-92a expression improved cardiac function as evidenced by increased EF and FSs, and decreased LVIDd and LVIDs (p&#x2009;<&#x2009;0.05). CONCLUSION: miR-92a may serve as a novel diagnostic and therapeutic biomarker for heart failure by altering cardiac remodeling.