Evidence map›Paper›PMID 42776477›Full record

ArticleJournal of thrombosis and thrombolysis2026

miR-224-5p alleviates oxygen-glucose deprivation/reperfusion injury via regulating FAS.

Yanping Zhu, Haitao Fang, Yawen Zhang, Yu Zhang

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Article in Journal of thrombosis and thrombolysis, 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

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4 authors.

Yanping ZhuDepartment of Neurology III, Taiyuan People's Hospital, Taiyuan, 030025, China.
Haitao FangDepartment of Neurology, General Hospital of Shaoxing Central Hospital Medical Consortium, Shaoxing, 312030, China.
Yawen ZhangDepartment of Neurology, The Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.
Yu ZhangDepartment of Neurology, Central Hospital Affiliated to Shandong First Medical University, No.105, Jiefang Road, Lixia District, Jinan, 250013, Shandong Province, China. Zhangyu_neuro@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

miR-224-5p is downregulated in patients with cerebral infarction (CI); however, its diagnostic value and underlying mechanisms remain to be fully elucidated. The present investigation sought to explore the potential auxiliary diagnostic value of serum miR-224-5p between CI patients and healthy volunteers, and clarify its regulatory mechanism. Serum levels of miR-224-5p and FAS were quantified in CI patients via qRT-PCR. ROC curve analysis was utilized to evaluate the diagnostic efficacy of miR-224-5p in CI, while a binary logistic regression model was employed to identify variables associated with elevated CI risk. CCK-8, flow cytometry, and ELISA were employed to measure cell viability, apoptosis rate, and inflammatory factor levels, respectively. Bioinformatics analysis, coupled with a dual-luciferase reporter assay, was performed to validate the miR-224-5p target gene. miR-224-5p was markedly downregulated in CI patients, and this molecule showed moderate discriminatory ability to distinguish CI patients from healthy controls with an AUC of 0.827, which only reflects its differentiation efficiency versus healthy population rather than other neurological disorders. Reduced miR-224-5p expression, diabetes mellitus and hyperlipidemia were significantly linked to higher risk of CI. In the OGD/R cell model, miR-224-5p upregulation reversed the injury phenotypes, including decreased cell viability, increased apoptosis rate, and aggravated inflammatory response. miR-224-5p directly targets FAS. FAS exhibited marked overexpression in CI patient serum and bore a negative correlation with miR-224-5p expression. FAS overexpression elicited reduced cell viability, elevated apoptosis rate, and triggered an inflammatory response. Serum miR-224-5p could serve as a potential auxiliary biomarker for distinguishing CI patients from healthy individuals in single-center cohort; further multi-center validation and disease control groups are required to confirm its clinical diagnostic performance.

Indexed as

BiomarkerCerebral infarctionDiagnosisFASmiR-224-5p

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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.