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Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

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...
Mitral Regurgitation I: Introduction01:20

Mitral Regurgitation I: Introduction

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...
Mitral Stenosis I: Introduction01:22

Mitral Stenosis I: Introduction

Mitral Valve Stenosis (MVS) is a heart condition where the mitral valve narrows, impeding blood circulation from the left atrium to the left ventricle. The etiology and pathophysiology of this condition are multifaceted, leading to a cascade of cardiovascular complications.Causes of Mitral Valve StenosisRheumatic Heart Disease: It is the main cause of mitral valve stenosis, particularly in developing nations. This condition arises from rheumatic fever, an inflammatory illness resulting from...
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...

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Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
08:34

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Published on: September 25, 2017

FGF23 induces left ventricular hypertrophy.

Christian Faul1, Ansel P Amaral, Behzad Oskouei

  • 1Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA. cfaul@med.miami.edu

The Journal of Clinical Investigation
|October 12, 2011
PubMed
Summary
This summary is machine-generated.

Fibroblast growth factor 23 (FGF23) directly causes left ventricular hypertrophy (LVH) in chronic kidney disease (CKD). This FGF23-driven LVH occurs independently of klotho, suggesting new therapeutic targets for cardiovascular disease in CKD patients.

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Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice
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Area of Science:

  • Nephrology
  • Cardiology
  • Endocrinology

Background:

  • Chronic kidney disease (CKD) is a major public health issue linked to increased cardiovascular disease (CVD) mortality.
  • Left ventricular hypertrophy (LVH) is a key mechanism of CVD in CKD patients.
  • Elevated fibroblast growth factor 23 (FGF23) is associated with higher risks of LVH and mortality in CKD, but causality is unclear.

Purpose of the Study:

  • To investigate the causal role of FGF23 in the pathogenesis of LVH in CKD.
  • To explore the FGF23 signaling pathway in cardiac hypertrophy.
  • To determine if FGF23's effect on LVH is dependent on its coreceptor, klotho.

Main Methods:

  • Analysis of FGF23 levels and LVH in a diverse CKD cohort.
  • In vitro studies using isolated rat cardiomyocytes to assess FGF23 effects on hypertrophy via FGF receptor and calcineurin-NFAT pathways.
  • In vivo studies in wild-type and klotho-deficient mice involving FGF23 administration and FGF-receptor blocker treatment in a CKD model.

Main Results:

  • Elevated FGF23 levels were independently associated with LVH in CKD patients.
  • FGF23 induced pathological hypertrophy in rat cardiomyocytes through FGF receptor-dependent calcineurin-NFAT signaling, independent of klotho.
  • FGF23 administration caused LVH in mice; klotho-deficient mice exhibited elevated FGF23 and LVH.
  • FGF-receptor blockade attenuated LVH in a CKD animal model without affecting blood pressure.

Conclusions:

  • FGF23 plays a direct, klotho-independent causal role in the development of LVH in CKD.
  • Chronically elevated FGF23 contributes significantly to LVH and mortality rates in CKD patients.
  • Targeting the FGF23-FGF receptor pathway may offer a novel therapeutic strategy for mitigating cardiovascular risk in CKD.