ArticleCellular & molecular biology letters2025
M2 macrophage-derived extracellular vesicles protect against abdominal aortic aneurysm by modulating macrophage polarization through miR221-5p.
Article in Cellular & molecular biology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- NCOA4 Accelerates Abdominal Aortic Aneurysm Formation by Regulating Macrophage Activation and Ferroptosis via STAT1-CH25H Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Extracellular Vesicles as Biomarkers for Vascular Disease.Biomolecules · 2026Review
- Role of Extracellular Vesicles in Abdominal Aortic Aneurysm: Pathophysiology, Biomarkers, and Therapeutic Potentials.International journal of molecular sciences · 2026Review
- Extracellular vesicles for abdominal aortic aneurysm: mechanisms, therapeutic potential, and translational challenges.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Macrophage-derived CCL20 promotes abdominal aortic aneurysm progression via lymphocytes CCR6.Frontiers in immunology · 2026Article
- Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundExtracellular vesicles (EVs) derived from M2 macrophages (M2-EVs) play a protective role in the pathogenesis of acute lung injury. However, their roles and mechanisms in abdominal aortic aneurysm (AAA) are unknown.
methodsThe effects of M2-EVs in AAA were examined in ApoE
resultsM2-EVs significantly reduced AAA incidence and maximal aortic diameters, improved fiber continuity, increased α-SMA, and reduced macrophage infiltration in AAA mice. RNA sequencing revealed that miR221-5p was upregulated in M2-EVs and downregulated in AAA. miR221-5p-ASOs reduced the protection of M2-EVs in AAA mice. M2-EVs induced M2 macrophage polarization, while miR221-5p-ASOs had no effect. Moreover, M2-EVs alleviated oxidative stress and inflammatory responses in HAECs. Mechanistically, miR221-5p bound to poly(ADP-ribose) polymerase 1 (PARP-1) mRNA and reduced PARP-1 expression; PARP-1 was bound to protein phosphatase 1ɑ (PP-1ɑ) and negatively regulated its expression. In vitro experiments showed miR221-5p modulated macrophage polarization through the PARP-1/PP-1ɑ/JNK/c-Jun pathway. Macrophage deletion of PARP-1 inhibited AAA formation and phosphorylation of JNK/c-Jun in mice.
conclusionsmiR221-5p in M2-EVs plays a critical role in AAA pathophysiology by modulating macrophage polarization through PARP-1/PP-1ɑ/JNK/c-Jun signaling. M2-EVs and miR221-5p represent promising therapeutic options for AAA.
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