# Mechanisms and emerging research trends of angiogenesis promotion by small extracellular vesicles from different cellular sources in alleviating myocardial infarction injury

**Authors:** Lian Liu, Hang Hu, Yu Cao, Lu Gan

PMC · DOI: 10.3389/fphar.2026.1766323 · Frontiers in Pharmacology · 2026-03-16

## TL;DR

This review explores how small extracellular vesicles from different cell types help promote blood vessel growth to treat heart attack damage.

## Contribution

The paper systematically summarizes the roles of sEVs from various sources in promoting angiogenesis for myocardial infarction treatment.

## Key findings

- sEVs deliver bioactive molecules like miRNAs and cytokines to activate endothelial cell functions.
- sEVs from stem, immune, and cardiac cells enhance angiogenesis and reduce cardiac remodeling after MI.
- The review highlights recent advances in sEV-based strategies for improving MI prognosis.

## Abstract

Myocardial infarction (MI), a lethal coronary artery disease primarily triggered by atherothrombosis or an imbalance in myocardial oxygen supply and demand, stands as a leading cause of mortality worldwide. Promoting angiogenesis is recognized as an effective therapeutic strategy for MI, a process highly dependent on the functional status of endothelial cells (ECs). Small extracellular vesicles (sEVs), which are membrane-bound vesicles secreted by cells and enriched with bioactive molecules including proteins, lipids, and RNAs, are ubiquitously present in the secretome of diverse cell types such as stem cells, immune cells, and cardiac cells. Studies have confirmed that sEVs can deliver specific “cargo” such as miRNAs and cytokines via paracrine or endocrine pathways, activating key downstream signaling cascades. This effectively promotes EC proliferation, migration, and tube formation, thereby enhancing angiogenic capacity and ultimately mitigating pathological cardiac remodeling while improving prognosis post-MI. This review focuses on sEVs derived from various cellular sources, systematically summarizing their roles in promoting angiogenesis and the latest research advances in regulating EC function, aiming to provide novel insights for the effective treatment of MI.

## Linked entities

- **Diseases:** myocardial infarction (MONDO:0005068)

## Full-text entities

- **Diseases:** MI (MESH:D009203), coronary artery disease (MESH:D003324)
- **Chemicals:** oxygen (MESH:D010100), lipids (MESH:D008055)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13034055/full.md

## References

148 references — full list in the complete paper: https://tomesphere.com/paper/PMC13034055/full.md

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Source: https://tomesphere.com/paper/PMC13034055