Serum miR-224-5p distinguishes cerebral infarction from healthy controls with moderate accuracy
The study reports that serum miR-224-5p is significantly downregulated in patients with cerebral infarction and demonstrates moderate discriminatory ability against healthy volunteers, yielding an AUC of 0.827. In vitro models of oxygen-glucose deprivation/reperfusion injury show that restoring miR-224-5p levels mitigates cellular damage and inflammation by directly targeting FAS, which is concurrently overexpressed in patient serum. For laboratory diagnostics, these findings position miR-224-5p as a potential auxiliary biomarker, though the authors stress that multi-center validation and head-to-head comparison with other neurological disorders are required before clinical adoption.
The original study
miR-224-5p alleviates oxygen-glucose deprivation/reperfusion injury via regulating FAS.
- Authors
- Zhu Y, Fang H, Zhang Y, Zhang Y
- Journal
- Journal of thrombosis and thrombolysis
- Type
- Journal Article
- PMID
- 42776477
Original 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.