TGα2β-modified adipose-derived stem cell exosomes regulate collagen synthesis in fibroblasts and enhance chronic ulcerative wound repair through the ILK/AKT signaling pathway.

Authors

Qin Qi, Lifang Lu, Xueyan Nan

Published in

Pakistan journal of pharmaceutical sciences. Volume 39. Issue 11. Pages 3543-3553. Nov 01, 2026.

Abstract

Chronic ulcerative wounds, particularly diabetic foot ulcers, present a significant clinical challenge owing to their complex pathophysiology and limited response to conventional therapies. Although exosomes derived from adipose-derived mesenchymal stem cells (ADSC-exos) have shown promise in promoting tissue repair, the specific mechanisms underlying their effects, particularly their involvement in the integrin-linked kinase (ILK)/AKT signaling pathway, remain poorly elucidated.
This study aimed to elucidate whether exosomes from ADSCs modified with ITGα2β (ITGα2β-ADSC-exos) enhance chronic ulcerative wound healing by modulating fibroblast collagen synthesis via the ILK/AKT signaling axis.
ITGα2β-ADSC-exos were characterized using transmission electron microscopy, nanoparticle tracking analysis and Western blotting. Their effects on ILK/AKT pathway activation, migration and collagen production in fibroblasts were assessed in-vitro. For in-vivo validation, a diabetic rat model with full-thickness skin wounds was established and randomly allocated into five groups: Control (PBS), unmodified exosomes, ITGα2β-Modified exosomes (ITG-Exo), ITG-Exo co-administered with the ILK inhibitor QLT0267 and ITG-Exo co-administered with the AKT inhibitor MK-2206. Wound healing progression, histological changes, microvessel density (via CD31 immunohistochemistry) and the expression of pathway-related proteins (p-AKT, COL1A1, COL3A1) were evaluated.
ITGα2β modification enhanced the levels of characteristic markers and the yield of ADSC-exos. These modified exosomes potently activated the ILK/AKT pathway in fibroblasts, subsequently promoting fibroblast proliferation, migration and the synthesis of type I and III collagen. In diabetic rats, ITGα2β-ADSC-exos significantly accelerated wound closure, improved granulation tissue formation and increased microvessel density. Crucially, these therapeutic effects were entirely abrogated by co-administration of either the ILK inhibitor QLT0267 or the AKT inhibitor MK-2206, which instead exacerbated tissue vacuolization and inflammation. Western blot analysis confirmed that the pro-healing effects correlated with upregulation of p-AKT and collagen proteins.
ITGα2β-modified ADSC-exos regulate collagen synthesis in fibroblasts and facilitate chronic ulcerative wound healing via the ILK/AKT signaling pathway.

PMID:
42633542
Bibliographic data and abstract were imported from PubMed on 23 Aug 2026.

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