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<p>Treg dysfunction in ischemic cardiomyopathy (ICM) remains mechanistically unclear. We investigated ICM plasma small extracellular vesicles (ICM-sEVs) in Treg regulation and post-MI remodeling. Flow cytometry assessed Treg frequency. ICM-sEV miRNA sequencing revealed miR-223-3p enrichment, validated using miR-223<sup>−/−</sup> and Foxp3<sup>GFP/+</sup> mice. ICM patients and mice exhibited elevated Treg numbers but suppressed Foxp3. miR-223-3p was upregulated in ICM-sEVs and inversely correlated with functional Tregs. ICM-sEVs administration aggravated ventricular remodeling post myocardial infarction (MI) in mice while reducing Treg frequency and elevating miR-223-3p in vitro. miR-223 knockdown increased Treg cell number and Foxp3 expression, whereas miR-223 overexpression reversed the phenotype. ICM-sEVs aggravate ventricular remodeling post-MI and promote miR-223-3p-mediated Treg cell dysfunction.</p> Graphical Abstract <p>This study demonstrated a dysfunctional phenotype in Treg cells from ICM patients and probably correlated with miR-223-3p from ICM sEVs. ICM-sEVs aggravated ventricular remodeling after myocardial infarction and worsened cardiac function through dysfunctional Treg cells mediated by miR-223-3p</p> <p></p>

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Plasma Small Extracellular Vesicles of Ischemic Cardiomyopathy Aggravate Ventricular Remodeling Post-Myocardial Infarction and Promote miR-223-3p-mediated Dysfunction in Regulatory T Cells

  • 期刊论文

  • 发表日期：

    2025年5月8日

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  • Bifang Mai,
  • Wenlong Jiang,
  • Jing Yang,
  • Yuyang Chen,
  • Zhen Qin,
  • Yuan Li,
  • Wenqing Tu,
  • Yuhan Lin,
  • Wai Seng Chan,
  • Jianhua Wu,
  • Fangzhou Cheng,
  • Tao Xu,
  • Shuanglun Xie

摘要

Treg dysfunction in ischemic cardiomyopathy (ICM) remains mechanistically unclear. We investigated ICM plasma small extracellular vesicles (ICM-sEVs) in Treg regulation and post-MI remodeling. Flow cytometry assessed Treg frequency. ICM-sEV miRNA sequencing revealed miR-223-3p enrichment, validated using miR-223−/− and Foxp3GFP/+ mice. ICM patients and mice exhibited elevated Treg numbers but suppressed Foxp3. miR-223-3p was upregulated in ICM-sEVs and inversely correlated with functional Tregs. ICM-sEVs administration aggravated ventricular remodeling post myocardial infarction (MI) in mice while reducing Treg frequency and elevating miR-223-3p in vitro. miR-223 knockdown increased Treg cell number and Foxp3 expression, whereas miR-223 overexpression reversed the phenotype. ICM-sEVs aggravate ventricular remodeling post-MI and promote miR-223-3p-mediated Treg cell dysfunction.

Graphical Abstract

This study demonstrated a dysfunctional phenotype in Treg cells from ICM patients and probably correlated with miR-223-3p from ICM sEVs. ICM-sEVs aggravated ventricular remodeling after myocardial infarction and worsened cardiac function through dysfunctional Treg cells mediated by miR-223-3p