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 II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

519
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,...
519
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

454
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...
454
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

498
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...
498
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

374
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...
374
Cardiomyopathy I: Introduction and Classification01:25

Cardiomyopathy I: Introduction and Classification

552
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...
552
Cardiomyopathy VI: Nursing Management01:29

Cardiomyopathy VI: Nursing Management

333
Assessment: Nursing management of patients with cardiomyopathy begins with a thorough assessment of the patient's history, including a family history of cardiomyopathy or sudden cardiac death, personal history of heart disease, hypertension, diabetes, and any alcohol consumption or drug use.During the physical examination, assess vital signs, look for signs of heart failure (such as edema, jugular venous distention, and cyanosis), auscultate for abnormal heart sounds (like murmurs and gallops),...
333

You might also read

Related Articles

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

Sort by
Same author

Smartphone Instrumented 30-Second Chair Stand Recovers Body Composition and Strength Biomarkers.

Research square·2026
Same author

Distinct Proteasomal Pathways Drive Oncogenic PPM1D Activation.

bioRxiv : the preprint server for biology·2026
Same author

Multicenter dose de-escalation phase I trial of pressurized intraperitoneal aerosolized chemotherapy (PIPAC) nab-paclitaxel and cisplatin in combination with systemic nab-paclitaxel in recurrent ovarian cancer patients: trial in progress.

Pleura and peritoneum·2026
Same author

Sotatercept Reverses SIN3a Deficiency-Driven PAH by Reprogramming BMPR2/TGF-β-HIF-1α Signaling Pathways.

bioRxiv : the preprint server for biology·2026
Same author

Emerging trends and treatment strategies in ovarian cancer: A comprehensive review.

Critical reviews in oncology/hematology·2026
Same author

Long-Term Impact of Western Diet on Right Ventricular Transcriptome: Uncovering Sex-Specific Patterns in C57BL/6J Mice.

International journal of molecular sciences·2026

Related Experiment Video

Updated: Jan 25, 2026

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
06:22

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

Published on: November 29, 2024

1.4K

CXCR4 Cardiac Specific Knockout Mice Develop a Progressive Cardiomyopathy.

Thomas J LaRocca1, Perry Altman2, Andrew A Jarrah3

  • 1Cardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, NY 10128, USA. thomas.laRocca@mssm.edu.

International Journal of Molecular Sciences
|May 11, 2019
PubMed
Summary

CXCR4 knockout mice develop progressive cardiac dysfunction and heart failure by 12 months. Loss of CXCR4 leads to fibrosis, mitochondrial damage, and increased sensitivity to catecholamines, highlighting its role in regulating cardiac function.

Keywords:
CXCL12cardiomyopathychemokine receptor-4 (CXCR4)mitochondria

More Related Videos

In Vitro Generation of Heart Field-specific Cardiac Progenitor Cells
09:29

In Vitro Generation of Heart Field-specific Cardiac Progenitor Cells

Published on: July 3, 2019

6.7K
Isolation and Characterization of Cardiac Mesenchymal Stromal Cells from Endomyocardial Bioptic Samples of Arrhythmogenic Cardiomyopathy Patients
09:16

Isolation and Characterization of Cardiac Mesenchymal Stromal Cells from Endomyocardial Bioptic Samples of Arrhythmogenic Cardiomyopathy Patients

Published on: February 28, 2018

8.1K

Related Experiment Videos

Last Updated: Jan 25, 2026

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
06:22

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

Published on: November 29, 2024

1.4K
In Vitro Generation of Heart Field-specific Cardiac Progenitor Cells
09:29

In Vitro Generation of Heart Field-specific Cardiac Progenitor Cells

Published on: July 3, 2019

6.7K
Isolation and Characterization of Cardiac Mesenchymal Stromal Cells from Endomyocardial Bioptic Samples of Arrhythmogenic Cardiomyopathy Patients
09:16

Isolation and Characterization of Cardiac Mesenchymal Stromal Cells from Endomyocardial Bioptic Samples of Arrhythmogenic Cardiomyopathy Patients

Published on: February 28, 2018

8.1K

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Physiology

Background:

  • Cardiac hypertrophy and heart failure involve multiple signaling pathways.
  • CXCR4 negatively regulates beta-adrenergic receptor (β-AR) signaling, limiting calcium accumulation in cardiac myocytes.
  • CXCR4 knockout exacerbates hypertrophy and cardiac dysfunction under stress.

Purpose of the Study:

  • To investigate the structural and functional consequences of cardiomyocyte-specific CXCR4 knockout (CXCR4 cKO) in the absence of external stress.
  • To determine the role of CXCR4 in the development of cardiomyopathy and heart failure.

Main Methods:

  • Cardiac phenotype and function assessed via cardiac MRI, catheterization, and in vivo hemodynamics.
  • Histological analysis included cardiomyocyte dimensions, fibrosis, and mitochondrial morphology via electron microscopy.
  • Mice were studied at 2, 6, and 12 months of age, with and without isoproterenol (ISO) challenge.

Main Results:

  • CXCR4 cKO mice exhibited progressive cardiac dysfunction, leading to heart failure by 12 months.
  • Significant cardiac fibrosis and increased atrial naturietic factor (ANF) expression were observed at 6 months.
  • Mitochondrial derangements and heightened sensitivity to catecholamines (ISO) were noted in CXCR4 cKO mice.

Conclusions:

  • CXCR4 plays a crucial non-developmental role in maintaining cardiac function.
  • Loss of CXCR4 leads to progressive cardiomyopathy and heart failure, independent of exogenous stress.
  • CXCR4's negative regulation of β-AR signaling is vital for preventing cardiac dysfunction.