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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: Jun 30, 2026

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts

Published on: March 22, 2017

Single-cell transcriptomics reveals cell-type-specific diversification in human heart failure.

Andrew L Koenig¹, Irina Shchukina², Junedh Amrute¹

¹Center for Cardiovascular Research, Department of Medicine, Cardiovascular Division, Washington University School of Medicine, St. Louis, MO, USA.

Nature Cardiovascular Research

|August 12, 2022

Summary

This summary is machine-generated.

This study maps the cellular landscape of human heart failure using advanced single-cell RNA sequencing. It reveals distinct cell states and transcriptional changes in failing hearts, offering new insights into disease mechanisms.

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Published on: March 22, 2017

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Author Spotlight: Nuclei Isolation from Mouse Cardiac Progenitor Cells for Epigenome and Gene Expression Profiling at Single-Cell Resolution

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Published on: May 12, 2023

Area of Science:

Cardiovascular Biology
Genomics
Cellular and Molecular Medicine

Background:

Heart failure is a leading cause of global mortality.
Single-cell transcriptomics offers unprecedented resolution of cellular heterogeneity and gene expression.
Understanding the cellular basis of heart failure is crucial for developing effective therapies.

Purpose of the Study:

To define the cellular composition of the healthy and failing human heart.
To identify cell-specific transcriptional signatures associated with aging and heart failure.
To reveal disease-associated cell states and their impact on cardiac function.

Main Methods:

Integrated analysis of single-cell and single-nucleus RNA-sequencing data.
Data generated from 27 healthy donors and 18 individuals with dilated cardiomyopathy.
Comparative transcriptomic analysis to identify cell-type-specific changes.

Main Results:

Defined the cellular landscape of healthy and failing human hearts.
Identified cell-specific transcriptional signatures linked to age and heart failure.
Revealed distinct cellular responses: cardiomyocytes converge to disease states, while fibroblasts and myeloid cells diversify; endothelial cells and pericytes show global shifts.

Conclusions:

Provides a comprehensive cellular and transcriptomic atlas of human heart failure.
Identifies novel cell type-specific programs and disease-associated cell states.
Establishes a valuable resource for future heart failure research and therapeutic target identification.