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Platelet membrane-fusing MSC-derived apoptotic extracellular vesicles enhanced cardiac repair after

Zhifeng Song1, Fangshun Tan1, Yu Jiang2

  • 1Center for Coronary Heart Disease, Department of Cardiology, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Drug Delivery and Translational Research
|July 21, 2026
PubMed

Insights

Platelet membrane-modified vesicles enhance mesenchymal stem cell therapy for myocardial ischemia/reperfusion injury. This novel approach improves targeting and reduces cardiac damage without systemic toxicity.

Area of Science:

  • Cardiovascular Research
  • Regenerative Medicine
  • Biomaterials Engineering

Background:

  • Myocardial ischemia/reperfusion injury (I/RI) is a significant complication after acute myocardial infarction (AMI) interventions.
  • Mesenchymal stem cell-derived apoptotic vesicles (MSC-apoVs) offer cell-free therapy potential but lack effective in vivo targeting.
  • Current limitations hinder the therapeutic efficacy of MSC-apoVs for cardiac I/RI.

Purpose of the Study:

  • To engineer platelet membrane-modified apoVs (P-apoVs) for enhanced targeting to injured vascular and myocardial sites.
  • To evaluate the physicochemical properties and miRNA content of P-apoVs.
  • To assess the in vitro and in vivo therapeutic potential of P-apoVs in a myocardial I/RI model.

Main Methods:

  • Modification of MSC-apoVs with platelet membranes to create P-apoVs.
  • Physicochemical characterization and miRNA sequencing of P-apoVs.
  • In vitro assessment of cellular uptake, apoptosis inhibition, macrophage polarization, and endothelial cell function.
  • In vivo evaluation of P-apoV biodistribution, therapeutic efficacy, and toxicity in a myocardial I/RI rat model.

Main Results:

  • P-apoVs demonstrated favorable physicochemical properties with preserved miRNA content.
  • Enhanced cellular uptake of P-apoVs in macrophages, endothelial cells, and cardiomyocytes under stress conditions.
  • P-apoVs inhibited cardiomyocyte apoptosis, promoted M2 macrophage polarization, and improved endothelial cell function in vitro.
  • In vivo, P-apoVs preferentially accumulated in injured myocardium, attenuated cardiac remodeling post-I/RI, and showed no systemic toxicity.

Conclusions:

  • Platelet membrane modification significantly enhances the targeting and therapeutic efficacy of MSC-apoVs for myocardial I/RI.
  • P-apoVs represent a promising cell-free therapeutic strategy for mitigating cardiac I/RI.
  • This engineered vesicle approach holds potential for clinical translation in cardiovascular regenerative medicine.
Keywords:
Apoptotic vesiclesMyocardial ischemia/reperfusion injuryPlatelet-mimeticTargeted delivery

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