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Related Concept Videos

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

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...
Cellular Adaptation II: Hypertrophy01:26

Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...

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Related Experiment Video

Updated: May 27, 2026

Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization
08:22

Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization

Published on: September 15, 2018

Cardiac hypertrophy is positively regulated by MicroRNA miR-23a.

Kun Wang1, Zhi-Qiang Lin1, Bo Long1

  • 1Division of Cardiovascular Research, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.

The Journal of Biological Chemistry
|November 16, 2011
PubMed
Summary

MicroRNAs (miRNAs) regulate cardiac hypertrophy by targeting Foxo3a. This pathway, involving miR-23a and Foxo3a, offers potential therapeutic targets for heart failure treatment.

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In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
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Related Experiment Videos

Last Updated: May 27, 2026

Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization
08:22

Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization

Published on: September 15, 2018

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
09:53

In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge

Published on: June 15, 2018

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are key regulators of gene expression.
  • Cardiac hypertrophy is a precursor to heart failure.
  • Identifying miRNA targets in cardiac hypertrophy is crucial.

Purpose of the Study:

  • To investigate the role of miR-23a in cardiac hypertrophy.
  • To identify downstream targets of miR-23a in the heart.
  • To elucidate the miR-23a-Foxo3a axis in cardiac hypertrophic signaling.

Main Methods:

  • Generation of miR-23a transgenic mice.
  • Stimulation of cardiac hypertrophy via phenylephrine and transverse aortic banding.
  • Luciferase assays to confirm direct target interaction.
  • Analysis of Foxo3a and downstream gene expression.

Main Results:

  • miR-23a overexpression exacerbated cardiac hypertrophy.
  • miR-23a directly targets and suppresses transcription factor Foxo3a.
  • Foxo3a activation counteracted miR-23a-induced hypertrophy.
  • The miR-23a-Foxo3a pathway influences reactive oxygen species via manganese superoxide dismutase.

Conclusions:

  • miR-23a promotes cardiac hypertrophy by downregulating Foxo3a.
  • The miR-23a-Foxo3a axis is a significant component of the hypertrophic machinery.
  • This axis represents a potential therapeutic target for treating cardiac hypertrophy and heart failure.