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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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Updated: Jul 26, 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

Ythdf2 regulates cardiac remodeling through its mRNA target transcripts.

V Kmietczyk¹, J Oelschläger¹, P Gupta¹

¹Department of Internal Medicine III (Cardiology, Angiology, and Pneumology), Heidelberg University Hospital, 69120 Heidelberg, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, 69120 Heidelberg, Germany.

Journal of Molecular and Cellular Cardiology

|June 14, 2023

Summary

This summary is machine-generated.

The m6A reader protein Ythdf2 regulates cardiomyocyte function. Its deletion impairs heart function and increases fibrosis, revealing a novel mechanism for gene expression control in heart failure.

Keywords:

Eef2 Heart failure Translation Ythdf2 m(6)A

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Area of Science:

Cardiovascular Biology
Epigenetics
Molecular Cardiology

Background:

N6-methyladenosine (m6A) mRNA methylation is crucial for cardiomyocyte function.
Elevated m6A levels are observed in heart failure, but the role of m6A reader proteins remains unclear.

Purpose of the Study:

To investigate the role of the m6A reader protein Ythdf2 in cardiomyocyte function and heart failure.
To identify novel mechanisms by which m6A reader proteins regulate gene expression and cardiac function.

Main Methods:

In vivo studies involving cardiomyocyte-specific Ythdf2 deletion in mice.
In vitro knockdown of Ythdf2 in cardiomyocytes.
Cell type-specific Ribo-seq analysis to identify Ythdf2 targets.

Main Results:

Ythdf2 deletion in cardiomyocytes caused cardiac hypertrophy, reduced heart function, and increased fibrosis under pressure overload and aging.
Ythdf2 knockdown in vitro led to cardiomyocyte growth and remodeling.
Eukaryotic elongation factor 2 was identified as a direct target of Ythdf2-mediated post-transcriptional regulation.

Conclusions:

The m6A reader protein Ythdf2 plays a critical role in maintaining cardiomyocyte function and preventing cardiac dysfunction.
Ythdf2 regulates gene expression, including eukaryotic elongation factor 2, impacting cardiac remodeling and function.
This study enhances understanding of m6A methylation's regulatory role in cardiomyocytes and Ythdf2's control over cardiac function.