ArticleJournal of molecular histology2022
MiR-361-3p alleviates cerebral ischemia-reperfusion injury by targeting NACC1 through the PINK1/Parkin pathway.
Article in Journal of molecular histology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
The trial behind it
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- DICAR/DICAR-JP exerts therapeutic effects in brain stroke via the miR-361-5p/PRMT1 pathway.Frontiers in pharmacology · 2025Article
- Circular RNA CircFOXO3 Functions as a Competitive Endogenous RNA for Acid-Sensing Ion Channel Subunit 1 Mediating Oxeiptosis in Nucleus Pulposus.Biomedicines · 2024Article
- A Machine Learning Model Based on microRNAs for the Diagnosis of Essential Hypertension.Non-coding RNA · 2023Article
- The Role of microRNAs in Epigenetic Regulation of Signaling Pathways in Neurological Pathologies.International journal of molecular sciences · 2023Review
- MicroRNA-361-5p acts as a biomarker for carotid artery stenosis and promotes vascular smooth muscle cell proliferation and migration.BMC medical genomics · 2023Article
- Identification of distinct circulating microRNAs in acute ischemic stroke patients with type 2 diabetes mellitus.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Ischemic stroke is a nervous system disease with high rates of disability and mortality. MicroRNAs have been reported to modulate cerebral ischemia. The current study aimed to study the role of miR-361-3p in cerebral ischemia-reperfusion (I/R) injury. Experimental results revealed that miR-361-3p level was downregulated in a middle cerebral artery occlusion-induced ischemic stroke mouse model and in oxygen-glucose deprivation/reoxygenation-stimulated SH-SY5Y cells. After overexpressing miR-361-3p, the percentage of brain infarct volume and neurobehavioral scores in mice were significantly reduced, and the neuronal apoptosis was inhibited. Moreover, miR-361-3p overexpression could limit the production of reactive oxygen species (ROS). Furthermore, we investigated the underlying molecular mechanisms of miR-361-3p and identified that miR-361-3p combined with NACC1 3'UTR to negatively modulate its expression. In addition, NACC1 interacts with the PINK1/Parkin pathway in neurons. NACC1 overexpression could rescue the impacts of miR-361-3p mimics on cell apoptosis, ROS production and the PINK1/Parkin pathway. In conclusion, miR-361-3p could improve ischemia brain injury by targeting NACC1 through the PINK1/Parkin pathway. Therefore, miR-361-3p may serve as a potential therapeutic target for the brain injury after I/R.
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Registered trials
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.