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

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

Abstract read

In one paragraph

Article in Drug delivery and translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Lihong ZhangDepartment of Neurointervention and Neurocritical Care, Dalian Central Hospital, Dalian University of Technology (Dalian Central Hospital), No. 826, Xi'nan Road, Shahekou District, Dalian, 116033, China.

Cui WangDepartment of Neurology, Dalian Central Hospital Affiliated to Dalian University of Technology (Dalian Central Hospital), No. 826, Xi'nan Road, Shahekou District, Dalian City, 116033, Liaoning Province, China.

Zhanjun WuSchool of Materials Science and Engineering, Dalian University of Technology, 2 Linggong Road, Ganjingzi District, Dalian City, 116000, Liaoning Province, China.

Hong QuBidding and Procurement Office, The Second Affiliated Hospital of Dalian Medical University, No. 467 Zhongshan Road, Shahekou District, Dalian City, 116027, Liaoning Province, China.

Jitong MaSchool of Information Science and Technology, Dalian Maritime University, 1 Linghai Road, Dalian, 116026, China.

Di LiDepartment of Neurointervention and Neurocritical Care, Dalian Central Hospital, Dalian University of Technology (Dalian Central Hospital), No. 826, Xi'nan Road, Shahekou District, Dalian, 116033, China. lidi_0524@163.com.

Funding

the National Key Specialized Project. Funding Number: ZXYYGZD2402

6 · The paper itself

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.

Indexed as

EPCsExosomesFerroptosisInflammatory responseIntracranial atherosclerosisNCOA4/FTH1Neovascularization

Identifiers

PMID42603839

DOI10.1038/nature13148

What OpenQuestion holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.