ArticleMolecular neurobiology2025
Inhibition of DRP1-mediated Mitochondrial Fission and NRF2/HO-1/GPX4-mediated Ferroptosis by Mdivi-1 Protects Against Vascular Cognitive Impairment.
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 4 papers.
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4 citing papers in PubMed.
- Mitochondrial dynamics in environmental neurotoxicity: beyond oxidative stress toward spatial and functional reorganization.Archives of toxicology · 2026Review
- Microglial Activation Mediates Drp1-Dependent Mitochondrial Fission and Neuronal Apoptosis in a Lipopolysaccharide-Induced Model of Cognitive Dysfunction.Molecular neurobiology · 2026Article
- Sources of Oxidative Stress in Parkinson's Disease: Pathways and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondria as a therapeutic target in neurodegeneration caused by hypoxia and ischemia during the perinatal period.Pharmacological reports : PR · 2026Review
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Abstract
Vascular cognitive impairment (VCI), a consequence of chronic cerebral ischemia, is characterized by an insidious onset and challenging diagnosis. Ferroptosis is a recently identified form of iron-dependent, lipid peroxidation-mediated cell death, and is closely associated with mitochondrial function. While ferroptosis has been implicated in several neurological diseases, its role in VCI remains poorly understood. In this study, we investigated how modulating ferroptosis (ferrostatin-1), mitochondrial fission (Mdivi-1), and Nrf-2 (ML385) affected HT22 cells subjected to oxygen-glucose deprivation (OGD) via the measurement of ROS and caspase-3 levels. A rat model of VCI, induced by bilateral common carotid artery occlusion, was used to assess the effects of Mdivi-1 and ML385 on cognitive function (Morris water maze), neuronal apoptosis, ferroptosis, and the expression of mitochondrial fission-/fusion-related proteins (immunofluorescence and western blotting). Neural damage in the hippocampus and cortex was evaluated via hematoxylin and eosin staining. Mitochondrial ultrastructure and ROS levels were examined by transmission electron microscopy and dihydroethidium staining, respectively. Molecular docking was used to analyze Mdivi-1/Nrf-2 interaction. In vitro, ferrostatin-1 and Mdivi-1 reduced OGD-induced ROS accumulation and apoptosis, whereas ML385 exacerbated these effects. In vivo, Mdivi-1 improved VCI by reducing cortical injury, hippocampal apoptosis, and mitochondrial ultrastructural damage. This was achieved by inhibiting DRP1-dependent mitochondrial fission, promoting MFN1/2 expression, and activating Nrf-2/HO-1/GPX4 signaling, thereby suppressing oxidative stress and ferroptosis. However, ML385 reversed these effects. Molecular docking studies supported a direct interaction between Mdivi-1 and Nrf-2. Thus, targeting DRP1-mediated mitochondrial fission and Nrf-2/HO-1/GPX4-mediated ferroptosis offers a promising therapeutic strategy for VCI.
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