ArticleCell death & disease2021
Neuronal extracellular vesicle derived miR-98 prevents salvageable neurons from microglial phagocytosis in acute ischemic stroke.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 68 citations in OpenAlex.
- Extracellular Vesicles in Stroke: Drivers of Brain-Body Network Crosstalk.Translational stroke research · 2026Review
- Extracellular vesicles: Revolutionizing targeted therapy for ischemic stroke.Acta pharmaceutica Sinica. B · 2026Review
- Neurovascular Unit-Derived Extracellular Vesicles as Regulators of Post-Stroke Pathology and Neurorestoration.Biomolecules · 2026Review
- Targeting the Biology of Aging in Cerebrovascular Disease: Inflammation, Metabolism, Senescence, and Regeneration.International journal of molecular sciences · 2026Review
- Article
- Extracellular vesicle-derived miR-760 as a novel promising candidate biomarker differentiating stable RRMS from SPMS.Scientific reports · 2026Article
- Cellular Communication Networks Mediated by Microglia in Ischemic Stroke.CNS neuroscience & therapeutics · 2025Review
- Extracellular Vesicles as Therapeutic Strategy for Ischemic Stroke.Journal of neurochemistry · 2025Review
- Neuron-Derived Extracellular Vesicles: Emerging Regulators in Central Nervous System Disease Progression.Molecular neurobiology · 2025Review
- Role of extracellular vesicle-carried ncRNAs in the interactive 'dialogue' within the brain and beyond: emerging theranostic epigenetic modifiers in brain-derived nanoplatforms.Translational neurodegeneration · 2025Review
- The role of efferocytosis in ischemic stroke and insights from retinopathy.Trends in neurosciences · 2025Review
- Natural and engineered extracellular vesicles in vascular diseases: a focus on therapeutic effects, challenges and prospective.European journal of medical research · 2025Review
- Extracellular Vesicle-Derived miRNAs in Ischemic Stroke: Roles in Neuroprotection, Tissue Regeneration, and Biomarker Potential.Cellular and molecular neurobiology · 2025Review
- Knowledge mapping of exosomes in ischemic stroke: a bibliometric analysis.Frontiers in neurology · 2025Article
- Molecular Targeting of Ischemic Stroke: The Promise of Naïve and Engineered Extracellular Vesicles.Pharmaceutics · 2024Review
- Advancing stroke recovery: unlocking the potential of cellular dynamics in stroke recovery.Cell death discovery · 2024Review
- Lipidomic analysis identifies long-chain acylcarnitine as a target for ischemic stroke.Journal of advanced research · 2024Article
- Revolutionizing Ischemic Stroke Diagnosis and Treatment: The Promising Role of Neurovascular Unit-Derived Extracellular Vesicles.Biomolecules · 2024Review
- Exosomes as Vehicles for Noncoding RNA in Modulating Inflammation: A Promising Regulatory Approach for Ischemic Stroke and Myocardial Infarction.Journal of inflammation research · 2024Review
- Extracellular vesicles and their microRNA cargo in ischaemic stroke.The Journal of physiology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular vesicles (EVs), as a novel intercellular communication carrier transferring cargo microRNAs (miRNAs), could play important roles in the brain remodeling process after ischemic stroke. However, the detailed mechanisms involved in EVs derived miRNAs-mediated cellular interactions in the brain remain unclear. Several studies indicated that microRNA-98 (miR-98) might participate in the pathogenesis of ischemic stroke. Here, we showed that expression of miR-98 in penumbra field kept up on the first day but dropped sharply on the 3rd day after ischemic stroke in rats, indicating that miR-98 could function as an endogenous protective factor post-ischemia. Overexpression of miR-98 targeted inhibiting platelet activating factor receptor-mediated microglial phagocytosis to attenuate neuronal death. Furthermore, we showed that neurons transferred miR-98 to microglia via EVs secretion after ischemic stroke, to prevent the stress-but-viable neurons from microglial phagocytosis. Therefore, we reveal that EVs derived miR-98 act as an intercellular signal mediating neurons and microglia communication during the brain remodeling after ischemic stroke. The present work provides a novel insight into the roles of EVs in the stroke pathogenesis and a new EVs-miRNAs-based therapeutic strategy for stroke.
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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.