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Heart Failure II: Pathophysiology

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...

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Related Experiment Video

Updated: Dec 31, 2025

Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF

Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF

Published on: March 29, 2024

Seipin Knockout Mice Develop Heart Failure With Preserved Ejection Fraction.

Bo Bai^1,2, Wulin Yang^3,4, Yanyun Fu¹

¹Singapore Bioimaging Consortium, Agency for Science, Technology and Research, Singapore.

JACC. Basic to Translational Science

|January 8, 2020

Summary

This summary is machine-generated.

Lean diabetes can cause heart failure with preserved ejection fraction (HFpEF) in Asian patients. Lipodystrophic mice models reveal increased cardiac titin phosphorylation and fibrosis as potential therapeutic targets for HFpEF.

Keywords:

Ctrl, control (mice)EDPVR, end-diastolic pressure–volume relationship HFpEF, heart failure with preserved ejection fraction IQR, interquartile range LA, left atrial LV, left ventricular NET, neutrophil extracellular trap PEVK, proline, glutamate, valine, and lysine SKO, seipin knockout fibrosis heart failure with preserved ejection fraction neutrophil seipin titin

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Area of Science:

Cardiology
Metabolic Disorders
Animal Models

Background:

Lean diabetic patients in Asia experience poor clinical outcomes and reduced quality of life, particularly those with heart failure with preserved ejection fraction (HFpEF).
There is a critical need for appropriate animal models to investigate the mechanisms and develop novel therapies for this patient population.

Purpose of the Study:

To investigate whether lean diabetes can induce heart failure with preserved ejection fraction (HFpEF) characteristics.
To identify potential therapeutic targets for HFpEF in lean diabetic patients.

Main Methods:

Utilized lipodystrophic mice with seipin depletion, characterized by leanness and diabetes.
Assessed cardiac function and structure, focusing on titin phosphorylation, interstitial fibrosis, and neutrophil extracellular traps.
Correlated findings with clinical manifestations of HFpEF in Asian patients.

Main Results:

Lipodystrophic mice models successfully recapitulated major clinical manifestations of HFpEF.
Increased cardiac titin phosphorylation was observed.
Reactive interstitial fibrosis associated with neutrophil extracellular traps contributed to left ventricular stiffness.

Conclusions:

Lean diabetes itself can manifest as heart failure with preserved ejection fraction (HFpEF).
Elevated cardiac titin phosphorylation and fibrosis linked to neutrophil extracellular traps are key contributors to left ventricular stiffness in this condition.
These pathways represent promising therapeutic targets for Asian patients with HFpEF.