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Single-cell transcriptomic profiling reveals cell type heterogeneity between HFpEF and HFrEF.

Xingqi Xiao1, Wenqian Wu1, Qilong Mao1,2

  • 1State Key Laboratory of Respiratory Health and Multimorbidity, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.

Communications Biology
|October 7, 2025
PubMed
Summary
This summary is machine-generated.

This study reveals key differences in heart cells between heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). Cardiomyocytes are central communication hubs in HFpEF, with distinct subtypes and genetic regulation.

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Area of Science:

  • Cardiovascular Biology
  • Genomics
  • Systems Biology

Background:

  • Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome distinct from heart failure with reduced ejection fraction (HFrEF).
  • The cellular heterogeneity differences between HFpEF and HFrEF remain largely unknown.
  • Effective therapies for HFpEF are lacking.

Purpose of the Study:

  • To characterize cell type and subtype heterogeneity in HFpEF versus HFrEF.
  • To investigate cell-cell communication networks in HFpEF.
  • To explore genetic susceptibility underlying HFpEF and HFrEF.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) of 21,747 cardiac cells from HFpEF and HFrEF patients.
  • Cell-cell communication analysis.
  • Regulon analysis.
  • Integration of scRNA-seq, Genome-Wide Association Studies (GWAS), and expression quantitative trait loci (eQTL) data.

Main Results:

  • Cardiomyocytes, not endothelium or fibroblasts, are dominant communication hubs in HFpEF.
  • Significant heterogeneity exists in cardiomyocyte subtypes between HFpEF and HFrEF.
  • A specific HFpEF cardiomyocyte subtype shows altered fatty acid metabolism gene expression and elevated regulation of specific transcription factors (Ppargc1a, Atf6, E2f6, Mitf).
  • 210 HF susceptibility genes were identified and integrated with molecular data.

Conclusions:

  • This study provides a comprehensive atlas of cardiomyocyte differences in HFpEF and HFrEF.
  • Findings highlight the critical role of cardiomyocyte subtypes and communication in HFpEF.
  • Identified molecular targets offer potential therapeutic avenues for HFpEF and HFrEF.