ArticleMolecular neurobiology2025
Resveratrol Alleviates Diabetic Adipose Tissue-Derived Extracellular Vesicles-Induced Hippocampal Ferroptosis and Cognitive Dysfunction via Inhibiting miR-9-3p/SLC7A11 Axis.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Diagnostic and Predictive Value of Circulating and Exosomal microRNAs in Ferroptosis-Associated Neurological Conditions: A Systematic Review and Meta-analysis.Molecular neurobiology · 2026Pooled it
- Resveratrol Pretreatment and Decabromodiphenyl Ethane-Associated Hepatorenal Changes in a High-Dose Female Mouse Model: Redox Changes and Ferroptosis-Associated Markers.Food science & nutrition · 2026Article
- Catecholamine-mediated release of miR-133a-3p from adipocytes regulates the onset of chronic primary pain.The Journal of clinical investigation · 2026Article
- The Interaction Between Insulin Resistance and Neuroinflammation in the Brain and Its Impact on Diabetic Encephalopathy.Biology · 2026Review
- β-Caryophyllene confers protection against type 2 diabetic osteoporosis by blocking ferroptosis via the AMPK/Nrf2 pathway.Journal of pharmaceutical analysis · 2026Article
- The Role of Ferroptosis in Diabetes Pathogenesis: Therapeutic Implications of Hydrogen Sulfide and Its Reactive Metabolites.Antioxidants (Basel, Switzerland) · 2026Review
- Role and mechanisms of ferroptosis in cognitive impairment: From molecular pathways to therapeutic targets (Review).International journal of molecular medicine · 2026Review
- The Jekyll and Hyde of Extracellular Vesicles: Dual Roles as Disease Drivers and Therapeutic Saviors in Diabetic Brain.Molecular neurobiology · 2026Review
- Mechanisms and therapeutic strategies of ferroptosis in Diabetic-Associated Cognitive Dysfunction: focus on the crosstalk with apoptosis, autophagy, and pyroptosis.Molecular biology reports · 2026Review
- Research Progress on Pathology, Molecular Mechanisms, and Intervention Strategies of Cognitive Dysfunction Associated with Type 2 Diabetes.International journal of general medicine · 2026Review
- The diabetic retina-brain axis hypothesis in diabetic cognitive impairment: from pathophysiological mechanisms to therapeutic implications.Frontiers in endocrinology · 2026Review
- Ferroptosis in diabetes mellitus and its complications: overview of clinical and preclinical research.Cell death discovery · 2025Review
- Astragaloside IV Improves Cognitive Impairment by Reducing β-Amyloid and Tau Protein Deposition in Hippocampal Tissue of db/db Mice: A PET/CT Imaging-Based Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Nutritional strategies against dementia in rural populations.Frontiers in nutrition · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Visceral adipose tissue-derived extracellular vesicles (VAT-EVs) and their cargo miR-9-3p contribute to cognitive dysfunction and insulin resistance. Resveratrol (RES) prevents T2DM-induced cognitive impairment. This study investigates the interactive role of VAT-EVs and RES in diabetes-associated cognitive dysfunction (DACD) and the potential mechanisms. T2DM mice were constructed by high-fat diet (HFD)-feeding and streptozotocin (STZ) injection. Blood glucose and insulin levels evaluated the insulin resistance. Novel object recognition test (ORT) and Morris water maze (MWM) test assessed cognitive impairment. Nissl, H&E, and TUNEL stainings evaluated neuronal death. Immunofluorescence staining, immunostaining, DHE staining, Perls' staining, biochemical assays, and Western blots determined ER, oxidative stress, and ferroptosis. ELISA measured cytokines. VAT-EVs were isolated from adipose tissues of T2DM mice and characterized by transmission electron microscopy (TEM), Western blot, and dynamic light scattering detection. Treatment of resveratrol (RES) without or with miR-9-3p mimics investigated their interactive roles in DACD. Luciferase reporter assay, Western blot, and qRT-PCR validated the binding of miR-9-3p in SLC7A11. The blood glucose and insulin results and behavioral tests showed that T2DM mice exhibited insulin resistance and cognitive impairments. T2DM mice showed impaired structures, increased apoptosis, and enhanced inflammation, ER, oxidative stress, and ferroptosis in the hippocampus. RES diminished HFD-VAT-EVs-induced insulin resistance and cognitive declines through decreasing ER and oxidative stress, inflammation, and iron overload. Mechanistically, RES decreased miR-9-3p to upregulate SLC7A11 and subsequently mitigate ferroptosis. RES protected cognitive dysfunction and insulin resistance in T2DM via diminishing VAT-EVs and their cargo miR-9-3p-induced ER and oxidative stress, inflammation, and ferroptosis in the hippocampus.
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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.