Endothelial progenitor cells-derived exosomes reduce ferroptosis and promote neovascularization after intracranial atherosclerosis in association with the NCOA4/FTH1 cascade modulation.

Authors

Lihong Zhang, Cui Wang, Zhanjun Wu, Hong Qu, Jitong Ma, Di Li

Published in

Drug delivery and translational research. Aug 15, 2026. Epub Aug 15, 2026.

Abstract

Intracranial atherosclerosis (ICAS) is a leading cause of ischemic stroke. This study explored the mechanism of endothelial progenitor cells-derived exosomes (EPCs-exos) in ICAS. Rat EPCs were isolated, EPCs-exos were extracted and identified. A rat model of ICAS was established, and EPCs and EPCs-exos or lentiviral si-NCOA4 were injected into rats to observe the histopathological changes in cerebral microvessels, ferroptosis, angiogenesis, inflammatory indexes, and the NCOA4/FTH1 pathway. Hematoxylin and eosin staining was performed to observe the histopathology of cerebral microvascular tissue. EPCs were successfully isolated from rats and EPCs-exos were identified. EPC treatment inhibited the NCOA4/FTH1 pathway, hindered inflammatory responses and ferroptosis in ICAS rats, promoted neovascularization, and improved histopathology. EPCs-exos similarly reduced inflammatory responses and ferroptosis and promoted neovascularization in ICAS rats. In conclusion, EPCs‑exos reduce ferroptosis, attenuate inflammatory responses, and enhance cerebral neovascularization in ICAS rats in association with the NCOA4/FTH1 pathway modulation.

PMID:
42603839
Bibliographic data and abstract were imported from PubMed on 16 Aug 2026.

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