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Related Experiment Video

Updated: May 16, 2026

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples
14:39

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples

Published on: April 21, 2014

Single-Cell Analysis of Human Heart Failure With Preserved Ejection Fraction.

Virginia S Hahn1, Mark Chaffin2, Bridget Simonson2

  • 1Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD (V.S.H., S.C.J., A.S.M., M.R., K.S., D.A.K.).

Circulation Research
|May 15, 2026
PubMed
Summary

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This study analyzed heart failure with preserved ejection fraction (HFpEF) using single-nucleus RNA sequencing. HFpEF shows distinct cell-type-specific transcriptomic changes, particularly in cardiomyocytes, suggesting unique drivers for this condition.

Area of Science:

  • Cardiovascular Biology
  • Genomics
  • Molecular Pathology

Background:

  • Heart failure with preserved ejection fraction (HFpEF) is a complex multisystem disease with significant morbidity and mortality.
  • The precise pathobiology of HFpEF remains poorly understood, necessitating advanced molecular investigations.

Purpose of the Study:

  • To elucidate the cellular and molecular mechanisms underlying HFpEF.
  • To identify cell-type-specific transcriptomic alterations in the human HFpEF myocardium.
  • To compare HFpEF transcriptomic signatures with those of dilated cardiomyopathy.

Main Methods:

  • Single-nucleus RNA sequencing was performed on septal myocardial biopsies from HFpEF patients and nonfailing controls.
  • Nuclei were pooled, demultiplexed, and analyzed for gene expression quantification and cell type annotation.
Keywords:
cardiomyopathy, dilatedheart failuremetabolismmyocytes, cardiacsingle-cell analysis

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Last Updated: May 16, 2026

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  • Differential gene expression and pathway analyses were conducted to identify molecular differences between HFpEF and control groups.

    • Main Results:

    • 14 distinct cell types were identified, with numerous differentially expressed genes found across multiple cell types in HFpEF.
    • Common enriched pathways included immune activation, metabolism, and protein quality control, particularly between cardiomyocytes and fibroblasts.
    • HFpEF showed unique transcriptomic signatures in cardiomyocytes compared to dilated cardiomyopathy, with two genes (MAP2K6 and PLPP3) validated at the protein level.

    Conclusions:

    • The human HFpEF myocardium exhibits a unique, cell-type-specific transcriptomic landscape.
    • While sharing pathways with dilated cardiomyopathy, HFpEF has distinct cardiomyocyte alterations suggesting a specific pathological driver.
    • These findings offer a high-resolution map for identifying novel precision therapeutic targets for HFpEF.