ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Succinate Dehydrogenase Subunit A (SDHA) Mediated Microglia Extracellular Traps Formation Participating in Cerebral Ischemic Reperfusion Injury.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Review
- Comprehensive Evaluation of YJ-2 as a PAD4 Inhibitor in Alleviating Ischemic Brain Injury: From NETs-Induced Neurotoxicity to In Vivo Neuroprotection.CNS neuroscience & therapeutics · 2026Article
- Widely targeted metabolomics and machine learning identify succinate as a key metabolite in sepsis-associated encephalopathy.iScience · 2026Article
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.Frontiers in immunology · 2026Review
- Microglia-derived metabolites as novel signaling molecules: regulating neural circuit function, behavior, and their role in psychiatric disorders.Frontiers in cellular neuroscience · 2026Review
- Succinate Dehydrogenase Subunit A (SDHA) Mediated Microglia Extracellular Traps Formation Participating in Cerebral Ischemic Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
22 authors.
Funding
Abstract
Ischemia reperfusion (I/R) injury associated with recanalization therapy in acute ischemic stroke (AIS) exacerbates the initial brain damage. However, it remains a clinical challenge due to limited understanding of the underlying mechanisms of I/R injury. This study aims to investigate the mechanism of succinate dehydrogenase (SDH)-mediated succinate oxidation in microglia extracellular traps (MiETs) formation and neuronal injury after cerebra I/R injury. The results show that microglia are the main cell type producing extracellular traps (ETs) at 24 h at cerebral parenchyma after cerebral I/R. Additionally, oxygen glucose deprivation/re-oxygenation (OGD/R) could induce MiETs formation and increased level of mitochondrial reactive oxygen species (mtROS). Microglia switches toward glycolysis with enhanced SDH activity and upregulated expression of SDH subunit A (SDHA) during MiETosis. Dimethyl malonate (DMM), a competitive SDH inhibitor, could reduce MiETosis by inhibiting succinate oxidation and mtROS production during reperfusion. Furthermore, DMM is found to alleviate neuronal injury after OGD/R exposure and neurological behavior disorders after cerebral I/R, and the effect is similar to MiETosis inhibitor BB-Cl amidine. These findings reveal a novel functional state of microglia and the role of succinate oxidation in MiETosis after cerebral I/R and provide a novel potential target for the treatment of AIS.
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Registered trials
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