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

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

789
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...
789
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

803
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,...
803
Cardiomyopathy I: Introduction and Classification01:25

Cardiomyopathy I: Introduction and Classification

855
Cardiomyopathy, or CMP, is a group of diseases affecting the myocardial structure, impairing its ability to pump blood effectively. This condition can lead to arrhythmias, heart failure, or sudden cardiac death.Cardiomyopathies are classified into primary and secondary categories:Primary Cardiomyopathy refers to conditions involving only the heart muscle that are often idiopathic (of unknown cause) or genetic. They primarily affect the myocardium without the involvement of other systemic...
855
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

1.5K
Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
1.5K
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

909
Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
909
Epigenetic Regulation01:37

Epigenetic Regulation

4.3K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
4.3K

You might also read

Related Articles

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

Sort by
Same author

Challenges and recommendations in establishing national human diversity genomic projects.

Nature methods·2026
Same author

Predictive Biomarkers for Coronary Collateral Circulation Development After Myocardial Infarction.

International journal of molecular sciences·2026
Same author

SARS-CoV-2 wastewater genomic surveillance: approaches, challenges, and opportunities.

Genome biology·2026
Same author

Robust software development practices improve citations of RNA-seq tools.

bioRxiv : the preprint server for biology·2025
Same author

The systematic assessment of completeness of public metadata accompanying omics studies in the Gene Expression Omnibus data repository.

Genome biology·2025
Same author

The systematic assessment of completeness of public metadata accompanying omics studies in the Gene Expression Omnibus.

bioRxiv : the preprint server for biology·2025

Related Experiment Video

Updated: Apr 15, 2026

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
03:45

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Published on: August 8, 2022

4.4K

Epigenetics, Modifiers, and Molecular Noise: Rethinking Pathophysiology in Dilated and Hypertrophic Cardiomyopathies.

Miruna Mihaela Micheu1, Eugeniu Catlabuga2, Alexei Leahu2

  • 1Department of Cardiology, Clinical Emergency Hospital of Bucharest, 8, Calea Floreasca, 014461 Bucharest, Romania.

International Journal of Molecular Sciences
|April 14, 2026
PubMed
Summary
This summary is machine-generated.

Genetic factors and environmental influences create complex cardiomyopathies, challenging traditional views. Understanding this intricate genetic architecture is key for personalized treatments and better patient outcomes.

Keywords:
dilated cardiomyopathyepigeneticshypertrophic cardiomyopathymodifiermolecular noise

More Related Videos

An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level
06:02

An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level

Published on: November 2, 2020

6.3K
A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

10.5K

Related Experiment Videos

Last Updated: Apr 15, 2026

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
03:45

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Published on: August 8, 2022

4.4K
An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level
06:02

An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level

Published on: November 2, 2020

6.3K
A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

10.5K

Area of Science:

  • Cardiology
  • Genetics
  • Epigenetics

Background:

  • Cardiomyopathies are myocardial disorders with complex causes.
  • Traditional Mendelian genetics fail to explain variability in disease presentation and outcomes.
  • Emerging evidence points to a multifactorial etiology involving genetics, epigenetics, and environment.

Purpose of the Study:

  • To review the complex genetic architecture of hypertrophic and dilated cardiomyopathies.
  • To examine how epigenetic mechanisms, genetic modifiers, and molecular noise challenge classical pathophysiology.
  • To discuss the implications for risk stratification, genetic counseling, and personalized therapies.

Main Methods:

  • Literature review focusing on hypertrophic and dilated cardiomyopathies.
  • Critical analysis of genetic, epigenetic, and environmental factors.
  • Examination of molecular noise and its role in disease manifestation.

Main Results:

  • Cardiomyopathy development is influenced by rare variants, common genetic variation, epigenetics, and environmental factors.
  • These factors contribute to significant phenotypic heterogeneity, disease severity, and progression.
  • Classical pathophysiology concepts are challenged by this complex interplay.

Conclusions:

  • A multilayered genetic architecture underlies cardiomyopathies.
  • This understanding is crucial for refined risk stratification and improved genetic counseling.
  • Personalized and potentially variant-agnostic therapeutic strategies can be developed.