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Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...

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In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
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Published on: June 15, 2018

MicroRNA-300-3p promotes cardiac hypertrophy by modulating the ACOX-1/GPX4 pathway.

Xiaojuan Li1, Yanjia Wang2, Ziyao Yang3

  • 1Department of Critical Care Medicine, People's Hospital of Ningxia Hui Autonomous Region, Yinchuan, China.

Biochemical and Biophysical Research Communications
|June 16, 2026
PubMed
Summary

MicroRNAs regulate cardiac hypertrophy (CH) by targeting ACOX1, promoting ferroptosis. DNMT1-mediated hypomethylation of miR-300-3p enhances this process, revealing a novel pathway for CH therapeutics.

Keywords:
ACOX1Cardiac hypertrophyDNA methylationFerroptosismiR-300-3p

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Epigenetics

Background:

  • Cardiac hypertrophy (CH) is a critical factor in heart failure development.
  • MicroRNAs (miRNAs) are implicated in cardiovascular diseases, but their role in CH requires further elucidation.
  • Understanding molecular mechanisms of CH is vital for therapeutic advancements.

Purpose of the Study:

  • To investigate the role of miR-300-3p in angiotensin II (Ang II)-induced cardiac hypertrophy.
  • To identify the molecular targets and pathways regulated by miR-300-3p in CH.
  • To explore the epigenetic regulation of miR-300-3p in the context of CH.

Main Methods:

  • In vitro studies using cell models of Ang II-induced CH.
  • Analysis of miR-300-3p targeting of ACOX1 using luciferase assays and Western blotting.
  • Assessment of ferroptosis markers and cell viability.
  • Investigation of DNMT1-mediated promoter methylation of miR-300-3p.
  • In vivo validation of the miR-300-3p/ACOX1/GPX4 axis.

Main Results:

  • miR-300-3p directly targets and downregulates ACOX1, promoting ferroptosis in Ang II-induced CH.
  • Overexpression of ACOX1 counteracted the effects of miR-300-3p, reducing ferroptosis and hypertrophy.
  • DNMT1-mediated hypomethylation of the miR-300-3p promoter increased its expression, contributing to CH.
  • ACOX1 demonstrated anti-hypertrophic effects through the GPX4 signaling pathway.

Conclusions:

  • DNMT1-regulated promoter hypomethylation enhances miR-300-3p expression, which suppresses ACOX1 and promotes ferroptosis in Ang II-induced CH.
  • The identified miR-300-3p/ACOX1/GPX4 signaling axis provides novel molecular insights into CH.
  • This pathway represents a potential therapeutic target for managing CH and preventing heart failure progression.