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Related Experiment Video

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Preparation of a Non-Cardiomyocyte Cell Suspension for Single-Cell RNA Sequencing from a Post-Myocardial Infarction Adult Mouse Heart
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Integrative Single-Cell Analysis Dissects the Transcriptomic Remodeling and Altered Interaction Networks of

Mingzhen Cao1,2, Da Ke1,2, Dan Huang1,2

  • 1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 19, 2025
PubMed
Summary

This study reveals how endothelial cell diversity changes after myocardial infarction (MI). Targeting the Mif-Cd44 interaction in tip-like cells could improve heart function post-MI.

Keywords:
endothelial cellsimmune cellmyocardial infarctionsingle‐cell analysis

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Single-cell Genomics

Background:

  • Myocardial infarction (MI) causes significant mortality, with vascular contributions poorly understood.
  • Endothelial cell diversity and function in cardiac injury require further characterization.

Purpose of the Study:

  • To characterize endothelial cell reprogramming following MI using single-cell transcriptomics.
  • To identify key endothelial cell-immune cell interactions and their role in cardiac dysfunction.

Main Methods:

  • Integrated multi-timepoint mouse cardiac single-cell RNA sequencing data.
  • Utilized scVelo, CellRank, and Dynamo for endothelial cell differentiation trajectory analysis.
  • Performed in silico simulations and in vivo pharmacological inhibition experiments.

Main Results:

  • Detailed transcriptome reprogramming of endothelial cell subsets post-MI.
  • Identified a critical Mif-Cd44 interaction between tip-like cells and monocytes in acute MI.
  • In silico Sox17 depletion simulation altered tip-like to capillary endothelial cell transition.
  • In vivo Mif inhibition worsened cardiac dysfunction in a mouse MI model.

Conclusions:

  • Endothelial cell heterogeneity plays a crucial role in the response to myocardial infarction.
  • The Mif-Cd44 pathway represents a potential therapeutic target for mitigating cardiac dysfunction after MI.