Single-cell and spatial transcriptomic analyses reveal the dynamic transcript profiles of myocardial

Jiaqi He1,2, Dali Zhang2, Haixu Song2

  • 1Graduate School, Army Medical University, Chongqing 400038, China.

PubMed

Insights

This study reveals distinct subtypes of cardiac lymphatic endothelial cells (LECs) in infarcted hearts, each with unique roles in inflammation, injury, and edema resolution following myocardial infarction (MI). These findings highlight the functional diversity of LECs in cardiac repair.

Area of Science:

  • Cardiovascular Biology
  • Lymphatic System Research
  • Regenerative Medicine

Background:

  • Cardiac lymphatic endothelial cells (LECs) are crucial in myocardial edema and inflammation.
  • The heterogeneity and specific functions of cardiac LECs remain largely unexplored.

Purpose of the Study:

  • To investigate the heterogeneity and functional roles of cardiac lymphatic endothelial cells (LECs) post-myocardial infarction (MI).
  • To map the spatial distribution and functional specialization of different LEC subtypes within the infarcted heart.

Main Methods:

  • Integration of single-cell and spatial transcriptome data from mouse hearts after MI.
  • Application of clustering, spatial localization, cell trajectory, and Cell-Chat analyses to identify LEC subtypes and functions.

Main Results:

  • Identification of four distinct subtypes of cardiac LECs with specific spatial localizations and functions.
  • LEC subtypes implicated in metabolic stress (LEC CaIII), immune response (LEC CaII), and edema resolution (LEC CaI, LEC collection).
  • LEC-mediated regulation of myocardial edema via Aquaporin 1 and macrophage infiltration via galectin-9 (Gal-9)-CD44 pathway.

Conclusions:

  • Cardiac LECs exhibit dynamic transcriptional heterogeneity and regional functional specialization post-MI.
  • Distinct LEC functional subgroups contribute differently to myocardial tissue repair and pathology.
  • Understanding LEC heterogeneity offers insights into therapeutic strategies for cardiac injury.
Abstract

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