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Pathophysiology of Heart Failure

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...

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Related Experiment Video

Updated: May 21, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

Spleen-Heart Cross-Talk Through CD23-Mediated Signal Promotes Cardiac Remodeling.

Yufan Feng¹, Yang Yang¹, Hongqin Yang¹

¹Department of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).

Circulation Research

|May 20, 2025

Summary

This study reveals that elevated lactotransferrin (Ltf) from the heart upregulates ADAM10, decreasing CD23 and increasing IgE in pathological cardiac remodeling. This Ltf-ADAM10-CD23 axis offers novel therapeutic targets for heart conditions.

Keywords:

heart failure immunoglobulin E spleen

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Cardiac Spheroids as in vitro Bioengineered Heart Tissues to Study Human Heart Pathophysiology

Cardiac Spheroids as in vitro Bioengineered Heart Tissues to Study Human Heart Pathophysiology

Published on: January 23, 2021

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Last Updated: May 21, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

Cardiac Spheroids as in vitro Bioengineered Heart Tissues to Study Human Heart Pathophysiology

Cardiac Spheroids as in vitro Bioengineered Heart Tissues to Study Human Heart Pathophysiology

Published on: January 23, 2021

Area of Science:

Immunology
Cardiology
Molecular Biology

Background:

Elevated immunoglobulin E (IgE) levels are linked to pathological cardiac remodeling.
The precise origin and production mechanisms of IgE in this context remain largely unknown.

Purpose of the Study:

To investigate the source of IgE and the underlying mechanisms of its production during pathological cardiac remodeling.
To explore the role of the IgE receptor CD23 and identify key signaling molecules involved in cardiac-spleen cross-talk.

Main Methods:

Flow cytometry was used to analyze IgE-producing B cells in various tissues of mice with transverse aortic constriction (TAC)-induced cardiac remodeling.
Genetic manipulation of CD23 (loss-of-function and gain-of-function) and administration of CD23-neutralizing antibodies were employed.
Proteomic analysis and ELISAs identified key molecular players in organ cross-talk regulating IgE production.

Main Results:

Splenic IgE-producing cells and IgE levels significantly increased in TAC mice, correlating with decreased CD23 expression.
Loss of CD23 exacerbated cardiac remodeling and IgE synthesis, while CD23 overexpression alleviated these effects.
Lactotransferrin (Ltf), released from the heart, was identified to upregulate ADAM10, leading to CD23 cleavage and increased IgE production. Ltf levels correlated with cardiac remodeling severity and IgE levels in mice and human heart failure patients.

Conclusions:

The lactotransferrin-ADAM10-CD23 axis is crucial for regulating IgE production via heart-spleen communication.
This axis represents a potential therapeutic target for managing IgE-mediated pathological cardiac remodeling.