# MiR-133b-3p attenuates angiotensin II-induced cardiac hypertrophy through the inhibition of apoptosis by targeting CDIP1 : MiR-133b-3p attenuates angiotensin II-induced cardiac hypertrophy

## TL;DR

MiR-133b-3p reduces heart enlargement caused by angiotensin II by preventing cell death through targeting CDIP1.

## Contribution

Identifies miR-133b-3p as a novel inhibitor of cardiac hypertrophy by targeting CDIP1.

## Key findings

- MiR-133b-3p expression is significantly reduced in Ang II-induced cardiac hypertrophy models.
- Overexpression of miR-133b-3p reverses Ang II-induced hypertrophy and apoptosis.
- CDIP1 is confirmed as a direct target of miR-133b-3p, and its silencing mimics the protective effects of miR-133b-3p.

## Abstract

MicroRNAs (miRNAs) have emerged as essential regulators that play important roles in the development of multiple systems. Recent studies have identified significant roles for miRNAs in the progression of cardiac hypertrophy. This study aims to investigate the effects of miR-133b-3p on angiotensin II (Ang II)-induced cardiac hypertrophy and apoptosis, as well as explore its underlying mechanisms. Our experimental results reveal that miR-133b-3p expression is significantly decreased in both animal and cell models of cardiac hypertrophy induced by Ang II. Overexpression of miR-133b-3p reverses the hypertrophic manifestations and apoptosis induced by Ang II. Through bioinformatics analysis and dual-luciferase reporter assays,
CDIP1 (cell death inducing p53 target 1) is identified as a direct target of miR-133b-3p, and the overexpression of miR-133b-3p reduces
CDIP1 expression. Additionally,
CDIP1 silencing suppresses cardiomyocyte hypertrophy and apoptosis induced by Ang II. In summary, these results suggest that miR-133b-3p may serve as a potential diagnostic marker for cardiac hypertrophy and that the upregulation of miR-133b-3p inhibits cardiac hypertrophy by targeting
CDIP1.