ArticleExperimental brain research2021
Mdivi-1 alleviates brain damage and synaptic dysfunction after intracerebral hemorrhage in mice.
Article in Experimental brain research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Effects of Mdivi‑1 on Mitochondrial Fission and Fusion Proteins in Hippocampal Granule Neurons in Kainate-Induced Injury.Bulletin of experimental biology and medicine · 2026Article
- Mitochondrial homeostasis imbalance-triggered PANoptosis in traumatic brain and spinal cord injury: from mechanism to therapeutic strategies.Redox biology · 2026Review
- Article
- Modulation of mitochondrial dysfunction: Mechanisms and strategies for the use of natural products to treat stroke.Neural regeneration research · 2026Article
- Histone lactylation leads to perioperative neurocognitive disorders by promoting the expression of Ralbp1 and inducing excessive mitochondrial fission in hippocampal neurons.Cellular and molecular life sciences : CMLS · 2026Article
- Lipoteichoic Acid Stimulation of Macrophages Causes Mitochondrial Dysfunction.International dental journal · 2026Article
- Inhibition of SIRT1/PGC-1α Axis Exacerbates Fluorine and Aluminium Induced Neurotoxicity via Drp1-dependent Aggravated Mitochondrial Fission.Molecular neurobiology · 2025Article
- Article
- Mitochondrial Quality Control: Insights into Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2025Review
- Nicotinamide N-oxide Inhibits Microglial Pyroptosis by Upregulating Mitophagy and Alleviates Neural Damage in Rats after TBI.Inflammation · 2025Article
- Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy.Frontiers in pharmacology · 2025Article
- GSDMD/Drp1 signaling pathway mediates hippocampal synaptic damage and neural oscillation abnormalities in a mouse model of sepsis-associated encephalopathy.Journal of neuroinflammation · 2024Article
- Review
- Mechanism and treatment of intracerebral hemorrhage focus on mitochondrial permeability transition pore.Frontiers in molecular neuroscience · 2024Review
- MSCs overexpressing GDNF restores brain structure and neurological function in rats with intracerebral hemorrhage.Molecular biomedicine · 2023Article
- Disrupted brain mitochondrial morphology after in vivo hydrogen sulfide exposure.Scientific reports · 2023Article
- Mdivi-1 Rescues Memory Decline in Scopolamine-Induced Amnesic Male Mice by Ameliorating Mitochondrial Dynamics and Hippocampal Plasticity.Molecular neurobiology · 2023Article
- Pterostilbene attenuates microglial inflammation and brain injury after intracerebral hemorrhage in an OPA1-dependent manner.Frontiers in immunology · 2023Article
- Mitophagy and Traumatic Brain Injury: Regulatory Mechanisms and Therapeutic Potentials.Oxidative medicine and cellular longevity · 2023Review
- Pharmacological Targeting of Mitochondrial Fission and Fusion Alleviates Cognitive Impairment and Brain Pathologies in Pre-diabetic Rats.Molecular neurobiology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
As a selective inhibitor of mitochondrial fission protein dynamin-related protein-1 (Drp1), mitochondrial division inhibitor 1 (mdivi-1) can cross the blood-brain barrier (BBB) and exert neuroprotection. However, it remains unclear whether mdivi-1 can attenuate intracerebral hemorrhage (ICH)-induced secondary brain injury. This study was undertaken to characterize the roles of mdivi-1 in short-term and long-term behavioral outcomes, along with synaptic plasticity changes in mice after ICH. The results indicated mdivi-1 reversed Drp1 translocation and the morphologic changes of mitochondria, as well as ameliorated short-term neurobehavioral deficits, the BBB disruption and brain edema remarkably. In addition, mdivi-1 could rescue ICH-induced motor and memory dysfunctions. Mdivi-1 could also prevent ICH-induced reductions in synaptic proteins (synapsin I, PSD95) and phosphorylated cAMP-response element binding (p-CREB). In vitro, mdivi-1 inhibited hemin-induced hippocampal neuron death and improved neurite outgrowth. In conclusion, we found that mdivi-1 can alleviate short-term and long-term neurological deficits, synaptic dysfunction. These findings demonstrate that mdivi-1 may be beneficial in the treatment of secondary brain injury, synaptic dysfunction and neurological outcomes caused by ICH.
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