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

1.1K
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...
1.1K
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

578
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...
578
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

658
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...
658
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

4.2K
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
4.2K
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

551
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...
551
Mitral Regurgitation I: Introduction01:20

Mitral Regurgitation I: Introduction

759
Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
759

You might also read

Related Articles

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

Sort by
Same author

[Systemic pruritus: focus on hematological, nephrogenic, and hepatobiliary etiologies].

Dermatologie (Heidelberg, Germany)·2026
Same author

The effects of elevated phosphate on the kidney - damaging the gatekeeper.

Pflugers Archiv : European journal of physiology·2026
Same author

Fluorine-18-Labeled Nucleotide Analogs Targeting Ecto-5'-Nucleotidase (CD73) for Positron Emission Tomography Imaging of Solid Tumors.

Angewandte Chemie (International ed. in English)·2026
Same author

Authors' Reply: Creatinine-Normalized Phosphaturia after Phosphate Loading in Skeletal Muscle-Specific Fgf23 Knockout Mice.

Journal of the American Society of Nephrology : JASN·2026
Same author

Cardiovascular Outcomes among New Users of GLP-1 Receptor Agonists Compared with DPP-4 Inhibitors and Sulfonylureas in Kidney Failure.

Journal of the American Society of Nephrology : JASN·2026
Same author

Effect of Clazakizumab on Neutrophil-Lymphocyte Ratio in Patients Receiving Hemodialysis: Secondary Analysis of the POSIBIL6ESKD Phase 2b Trial.

Clinical journal of the American Society of Nephrology : CJASN·2026

Related Experiment Video

Updated: Mar 2, 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

25.7K

FGF23/FGFR4-mediated left ventricular hypertrophy is reversible.

Alexander Grabner1,2, Karla Schramm1,3, Neerupma Silswal4

  • 1Katz Family Drug Discovery Center and Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA.

Scientific Reports
|May 18, 2017
PubMed
Summary

Fibroblast growth factor 23 (FGF23) causes cardiac hypertrophy, but this effect is reversible. Blocking FGF receptor 4 (FGFR4) reduces left ventricular hypertrophy in chronic kidney disease and aging models.

More Related Videos

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
07:26

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents

Published on: July 14, 2021

5.6K
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

7.8K

Related Experiment Videos

Last Updated: Mar 2, 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

25.7K
Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
07:26

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents

Published on: July 14, 2021

5.6K
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

7.8K

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Nephrology

Background:

  • Fibroblast growth factor 23 (FGF23) is a hormone linked to cardiac dysfunction in chronic kidney disease (CKD).
  • FGF23 targets cardiac myocytes via FGF receptor 4 (FGFR4), promoting left ventricular hypertrophy (LVH).
  • The reversibility of FGF23-induced cardiac effects and its role in aging-related cardiac remodeling are unclear.

Purpose of the Study:

  • To investigate the reversibility of FGF23-induced cardiac hypertrophy.
  • To determine the role of FGFR4 in CKD- and age-related LVH.
  • To explore the therapeutic potential of targeting FGF23/FGFR4 signaling in cardiac remodeling.

Main Methods:

  • In vitro and in vivo studies of FGF23-induced cardiac hypertrophy.
  • Utilizing the 5/6 nephrectomy rat model for CKD-induced LVH.
  • Employing aging mice and FGFR4 knockout mice to study age-related cardiac remodeling.
  • Assessing cardiac contractility and aortic relaxation.

Main Results:

  • FGF23-induced cardiac hypertrophy was reversible upon removal of the stimulus.
  • Specific blockade of FGFR4 attenuated established LVH in CKD rats.
  • Aging mice lacking FGFR4 were protected from LVH.
  • FGF23 increased cardiac contractility through FGFR4.

Conclusions:

  • FGF23/FGFR4 signaling plays a significant role in regulating cardiac remodeling and function.
  • Targeting cardiac FGF23/FGFR4 signaling may offer a protective strategy against CKD- and age-related LVH.