Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

867
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
867
Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

2.3K
Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
2.3K
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

346
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...
346
Co-activators and Co-repressors02:04

Co-activators and Co-repressors

8.3K
Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
8.3K
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

3.8K
Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
3.8K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Deletion of endothelial SOX9 reverses aging-induced cardiac dysfunction.

Cardiovascular research·2026
Same author

Lamin A/C-regulated cysteine catabolic flux modulates stem cell fate through epigenome reprogramming.

Nature metabolism·2026
Same author

Endothelial RNF20 suppresses endothelial-to-mesenchymal transition and safeguards physiological angiocrine signaling to prevent congenital heart disease.

Nature communications·2025
Same author

Decor(at)i(o)n: less is more?

Cardiovascular research·2025
Same author

Iron regulatory proteins secure iron availability in skeletal muscle to preserve exercise tolerance in heart failure.

Cardiovascular research·2025
Same author

AKT and heart remodelling: too much of a good thing?

European heart journal·2025

Related Experiment Video

Updated: Jan 5, 2026

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
08:34

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy

Published on: September 25, 2017

25.3K

Targeting cardiac hypertrophy through a nuclear co-repressor.

Andrea Grund1, Joerg Heineke1,2

  • 1Department of Cardiovascular Research, European Center for Angioscience (ECAS), Medical Faculty Mannheim, German Centre for Cardiovascular Research (DZHK, partner site Heidelberg/Mannheim), University of Heidelberg, Mannheim, Germany.

EMBO Molecular Medicine
|October 18, 2019
PubMed
Summary

Nuclear receptor co-repressor 1 (NCoR1) inhibits pathological cardiac hypertrophy by stabilizing the MEF2-HDAC complex. This finding reveals NCoR1 as a potential therapeutic target for heart failure and cardiac dysfunction.

More Related Videos

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

7.6K
Transverse Aortic Constriction in Mice
08:25

Transverse Aortic Constriction in Mice

Published on: April 21, 2010

68.8K

Related Experiment Videos

Last Updated: Jan 5, 2026

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
08:34

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy

Published on: September 25, 2017

25.3K
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

7.6K
Transverse Aortic Constriction in Mice
08:25

Transverse Aortic Constriction in Mice

Published on: April 21, 2010

68.8K

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Transcriptional Regulation

Background:

  • Heart failure is a critical condition where the heart cannot adequately pump blood.
  • Pathological cardiac hypertrophy is a major risk factor contributing to heart failure.
  • Understanding the molecular mechanisms underlying cardiac hypertrophy is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of the transcription co-repressor NCoR1 in regulating cardiac hypertrophy.
  • To elucidate the molecular mechanism by which NCoR1 influences cardiac function.
  • To identify NCoR1 as a potential therapeutic target for pathological cardiac hypertrophy.

Main Methods:

  • Investigated the interaction between NCoR1, MEF2, and class II HDACs.
  • Assessed the effect of NCoR1 on MEF2 transcriptional activity.
  • Evaluated the impact of NCoR1 on pathological cardiac hypertrophy and dysfunction in relevant models.

Main Results:

  • NCoR1 inhibits the transcriptional activity of MEF2 by stabilizing its complex with class II HDACs.
  • NCoR1 acts as a potent inhibitor of pathological cardiac hypertrophy.
  • NCoR1 plays a significant role in preventing cardiac dysfunction.

Conclusions:

  • NCoR1 is a key regulator of cardiac hypertrophy and function.
  • The mechanism involves NCoR1 stabilizing the MEF2-HDAC complex.
  • NCoR1 represents a promising therapeutic target for heart failure and related cardiac conditions.