ArticleOxidative medicine and cellular longevity2022
M1 Microglia Induced Neuronal Injury on Ischemic Stroke via Mitochondrial Crosstalk between Microglia and Neurons.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Mitochondrial Transfer in the Neurovascular Unit, Not Only for Energy Rescue: A Systematic Review.Aging and disease · 2024Pooled it
- Microglial Activation Under Hypoxic Conditions in Early Alzheimer's Disease: Can Natural SIRT1 Activators Be Therapeutic Allies in the Inflammation-Energy Axis?Phytotherapy research : PTR · 2026Review
- Intercellular Mitochondrial Transfer as Endogenous Neuroprotection: Mechanisms and Therapeutic Implications in Ischemic Stroke.Translational stroke research · 2026Review
- Resveratrol‒loaded self‒assembled tetrahedral framework nucleic acids reshape the epileptic microenvironment by regulating oxidative stress and neuroinflammation via the SIRT3/SOD2 pathway.Journal of nanobiotechnology · 2026Article
- Microglia-Neuron Crosstalk: An Intimate Molecular Conversation in Neurodegeneration.International journal of molecular sciences · 2026Review
- Recent Advances in Mitochondrial Transplantation for Ischemic Stroke: A Review of in Vitro and in Vivo Studies.Translational stroke research · 2026Review
- Insights gained from single-cell sequencing analysis of ischemic stroke.Frontiers in cell and developmental biology · 2026Review
- Microglial Polarization and Therapeutic Strategies in Post-stroke Neuroinflammation.Neurology and therapy · 2025Review
- Unlocking extracellular mitochondria from bench to clinical application in stroke.Stem cells translational medicine · 2025Review
- Ethanol Exposure Increases Oxygen Consumption by Developing Cerebral Arteries in a Trimester-, Concentration- and Sex-Dependent Manner.Biomolecules · 2025Article
- A Freely Moving Photothrombotic Stroke Model Reveals Sustained Dysfunction of GABAergic Neuron in Contralesional Cortex Using Miniaturized Two-Photon Microscopy.Translational stroke research · 2025Article
- ApTOLL ameliorates cognitive dysfunction and brain injury in ischemic stroke by regulating the miR-335-5p/IRAK1 axis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Bioactive Self-Assembled Nanoregulator Enhances Hematoma Resolution and Inhibits Neuroinflammation in the Treatment of Intracerebral Hemorrhage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Microglia-Astrocyte Crosstalk in Post-Stroke Neuroinflammation: Mechanisms and Therapeutic Strategies.Current neuropharmacology · 2025Review
- Review
- Therapeutic Potential of TPT-260 in Ischemic Stroke: An Investigation Into Its Anti-Inflammatory Effects and Impact on Microglial Activation.Journal of inflammation research · 2025Article
- Polyphenols: immunonutrients tipping the balance of immunometabolism in chronic diseases.Frontiers in immunology · 2024Review
- Perspective from single-cell sequencing: Is inflammation in acute ischemic stroke beneficial or detrimental?CNS neuroscience & therapeutics · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among the middle-aged and senile populations, ischemic stroke (IS) is a frequently occurring acute condition of the cerebrovascular system. Traditionally, it is recognized that when stroke occurs, microglia are activated into M1 phenotype and release cytotoxic cytokines, reactive oxygen species, proteases, and other factors, thus exacerbating the injury by further destroying or killing nearby neurons. In the latest research, the crucial role of the intercellular mitochondrial crosstalk on the stroke management has been demonstrated. Therefore, we tried to clarify mitochondrial crosstalk between microglia and neurons, and evaluated M1 microglial mitochondria-mediated neurological performance in transient middle cerebral artery occlusion (tMCAO) rats. We found that when microglia was activated into the proinflammatory M1 type after stroke, mitochondrial fission process was accelerated, and damaged mitochondria were released, further transferred to neurons and fused with neuronal mitochondria. As a result, the function of neuronal mitochondria was damaged by decreasing adenosine triphosphate (ATP), mitochondria membrane potential, and increasing excessive reactive oxygen species (ROS), thus inducing mitochondria-mediated neuronal death and finally aggravating ischemia injury. Taken together, it provides a novel neuroglial crosstalk mechanism at the mitochondrial level.
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