ArticleDisease markers2022
miR-602 Activates NRF2 Antioxidant Pathways to Protect HBMECs from OGD/R-Induced Oxidative Stress via Targeting KEAP1 and HRD1.
Article in Disease markers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Stent treatment improves cerebral microcirculatory disorder and blood-brain barrier function in internal carotid artery stenosis via intercellular adhesion molecule 1 modulation.Journal of cell communication and signaling · 2025Article
- MiRNA-Mediated Regulation of S100B: A Review.NeuroSci · 2025Review
- The study on circRNA profiling uncovers the regulatory function of the hsa_circ_0059665/miR-602 pathway in breast cancer.Scientific reports · 2024Article
- Review
- Melatonin alleviates oral epithelial cell inflammation via Keap1/Nrf2 signaling.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blood brain barrier (BBB) dysfunction is a critical complication of diabetes mellitus type 2 (T2DM), and the oxidative stress-induced apoptosis of human brain microvascular endothelial cells (HBMECs) is a main cause of BBB dysfunction. In this study, oxygen and glucose deprivation/reoxygenation (OGD/R) models were established with HBMECs to analyze the effects of miR-602 on the apoptosis of HMBECs. Western Blot, qRT-PCR, CCK-8, flow cytometry assay, ROS detection assay, and dual-luciferase reporter gene assay were used to measure the expression levels of corresponding factors and changes in intracellular environment. The results showed that miR-602 was overexpressed in HBMECs after OGD/R treatment, and miR-602 could reduce ROS level of OGD/R-induced HBMECs and promote cells survival via increasing the expression level of NRF2 and the transcription activity of NRF2/ARE. Besides, it was found that KEAP1 and HRD1 were downstream factors of miR-602, and the increase of both KEAP1 and HRD1 could reverse the effects of miR-602 on the OGD/R-induced HMBECs. Therefore, miR-602 may be a potential target for research and treatment of the oxidative stress injury induced by apoptosis in HMBECs.
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