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

618
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...
618
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

716
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,...
716

You might also read

Related Articles

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

Sort by
Same author

Glycolysis and hexosamine biosynthesis regulate inflammatory protein expression and maturation and key steps of monocyte recruitment by human aortic valve cells.

American journal of physiology. Heart and circulatory physiology·2026
Same author

Chemerin Activation of Toll-Like Receptor 4 Drives Mineralocorticoid Receptor-Mediated Aortic Valve Remodeling in Chronic Kidney Disease.

Journal of the American Heart Association·2026
Same author

Proteomic phenotyping with machine learning for cardiovascular outcomes in haemodialysis: insights from the AURORA trial.

European heart journal. Digital health·2026
Same author

Endogenous α-Klotho is a common target in atherosclerosis and calcific aortic valve disease.

Biochemical pharmacology·2026
Same author

Neutrophil Gelatinase-Associated Lipocalin Drives Cardiac Remodeling in Rats With Chronic Kidney Disease.

Hypertension (Dallas, Tex. : 1979)·2026
Same author

Erratum for Garcia et al., "Dual transcriptomic profiling of <i>Staphylococcus aureus</i> endocarditis in a porcine model reveals strong parallels with human infection".

mBio·2026

Related Experiment Video

Updated: Mar 17, 2026

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice
09:29

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

Published on: July 14, 2023

1.3K

Galectin-3, Cardiac Function, and Fibrosis.

Wouter C Meijers1, Natalia López-Andrés2, Rudolf A de Boer1

  • 1Department of Cardiology, University Medical Center Groningen, University of Groningen, RB Groningen, the Netherlands.

The American Journal of Pathology
|July 28, 2016
PubMed
Summary
This summary is machine-generated.

Galectin-3 in the heart may delay hypertrophy in pressure-overloaded conditions. This protein

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

10.7K
Refined CLARITY-Based Tissue Clearing for Three-Dimensional Fibroblast Organization in Healthy and Injured Mouse Hearts
07:10

Refined CLARITY-Based Tissue Clearing for Three-Dimensional Fibroblast Organization in Healthy and Injured Mouse Hearts

Published on: May 16, 2021

5.4K

Related Experiment Videos

Last Updated: Mar 17, 2026

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice
09:29

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

Published on: July 14, 2023

1.3K
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

10.7K
Refined CLARITY-Based Tissue Clearing for Three-Dimensional Fibroblast Organization in Healthy and Injured Mouse Hearts
07:10

Refined CLARITY-Based Tissue Clearing for Three-Dimensional Fibroblast Organization in Healthy and Injured Mouse Hearts

Published on: May 16, 2021

5.4K

Area of Science:

  • Cardiovascular Pathology
  • Molecular Cardiology

Background:

  • Investigates the role of Galectin-3 in pressure-overloaded heart remodeling.
  • Examines the impact of Galectin-3 on cardiac hypertrophy, survival, dysfunction, and fibrosis.

Discussion:

  • Corresponds to the findings by Frunza et al. regarding Galectin-3.
  • Highlights the association between Galectin-3 expression and cardiac remodeling.

Key Insights:

  • Myocardial Galectin-3 expression is linked to pressure-overloaded heart remodeling.
  • Galectin-3 may delay the hypertrophic response without negatively impacting survival or function.

Outlook:

  • Further research into Galectin-3's therapeutic potential in heart disease.
  • Understanding Galectin-3's precise mechanisms in cardiac adaptation.