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 II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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...
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 V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
Heart Failure I: Introduction01:27

Heart Failure I: Introduction

Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...

You might also read

Related Articles

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

Sort by
Same author

AI-driven discovery of GPNMB CAR T cells as a multi-cancer therapy.

Cell·2026
Same author

CAR-T cells targeting fibroblast activation protein eliminate pathological fibroblasts and preserve cardiac function in a Duchenne Muscular Dystrophy murine model.

Stem cell research & therapy·2026
Same author

Hopx(+) optic nerve head-astrocytes counter neuronal stress and glaucoma damage.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Anti-FAP CAR T cells produced in vivo reduce fibrosis and restore liver homeostasis in metabolic dysfunction-associated steatohepatitis.

Science translational medicine·2026
Same author

Reorganization of H3K9me2-modified chromatin regions during mouse embryonic development.

Developmental biology·2025
Same author

Epigenetic dysregulation of energy homeostasis drives aortic valve stenosis that is treatable with metformin.

JCI insight·2025
Same journal

AARS1 promotes tumor progression and immune evasion via ATF6 lactylation-mediated tryptophan metabolism in hepatocellular carcinoma.

Cell metabolism·2026
Same journal

Reactive species as regulators of immune cell metabolism, tolerance, and autoimmunity.

Cell metabolism·2026
Same journal

The interplay between the microbiome and immune cells in metabolic homeostasis and disease.

Cell metabolism·2026
Same journal

The metabolic basis of regulated cell death.

Cell metabolism·2026
Same journal

Gut microbiota-derived lysine phenylacetylation impairs mitochondrial function and is alleviated by SIRT3.

Cell metabolism·2026
Same journal

Methionine-supplemented longevity diet increases growth hormone, GLP-1, and FGF21; reduces frailty; and promotes healthspan.

Cell metabolism·2026
See all related articles

Related Experiment Video

Updated: Jun 5, 2026

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
07:31

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats

Published on: December 2, 2016

Heart-healthy hypertrophy.

Chinmay M Trivedi1, Jonathan A Epstein

  • 1Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.

Cell Metabolism
|January 4, 2011
PubMed
Summary
This summary is machine-generated.

Exercise stimulates heart muscle cell growth in mice, similar to humans. Molecular pathways involved in this cardiac myocyte proliferation may also contribute to harmful heart responses to stress.

More Related Videos

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
10:21

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

Published on: June 14, 2016

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

Related Experiment Videos

Last Updated: Jun 5, 2026

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
07:31

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats

Published on: December 2, 2016

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
10:21

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

Published on: June 14, 2016

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

Area of Science:

  • Cardiology
  • Molecular Biology
  • Exercise Physiology

Background:

  • Exercise is known to induce cardiac hypertrophy, an increase in heart muscle cell size.
  • Previous research has primarily focused on cardiomyocyte hypertrophy rather than proliferation in response to exercise.

Discussion:

  • This study investigates cardiac myocyte proliferation in mice following exercise.
  • The findings suggest that molecular regulators controlling exercise-induced cardiomyocyte proliferation are also implicated in maladaptive cardiac remodeling.
  • These pathways link beneficial exercise responses to pathological cardiac stress responses.

Key Insights:

  • Exercise triggers not only cardiomyocyte growth but also proliferation in mice.
  • Specific molecular pathways mediate exercise-induced cardiac myocyte proliferation.
  • These same pathways are associated with detrimental cardiac responses to stress, such as pressure overload.

Outlook:

  • Further research into these molecular regulators could identify therapeutic targets for heart disease.
  • Understanding the dual role of these pathways is crucial for differentiating adaptive and maladaptive cardiac remodeling.
  • This work opens new avenues for exploring exercise's complex effects on cardiovascular health.