Mir-30d Regulates Cardiac Remodeling by Intracellular and Paracrine Signaling.

ABSTRACT:

Rationale

Previous translational studies implicate plasma extracellular microRNA-30d (miR-30d) as a biomarker in left ventricular remodeling and clinical outcome in heart failure (HF) patients, although precise mechanisms remain obscure.

Objective

To investigate the mechanism of miR-30d-mediated cardioprotection in HF.

Methods and results

In rat and mouse models of ischemic HF, we show that miR-30d gain of function (genetic, lentivirus, or agomiR-mediated) improves cardiac function, decreases myocardial fibrosis, and attenuates cardiomyocyte (CM) apoptosis. Genetic or locked nucleic acid-based knock-down of miR-30d expression potentiates pathological left ventricular remodeling, with increased dysfunction, fibrosis, and cardiomyocyte death. RNA sequencing of in vitro

SUBMITTER: Li J 

PROVIDER: S-EPMC7790887 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature