ArticleResearch (Washington, D.C.)2026
Type 2 Diabetes Promotes the Microglial Pyroptosis by Activating NLRP3 Inflammasome to Impede Remyelination After Spinal Cord Injury.
Article in Research (Washington, D.C.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Diabetes hinders nerve recovery after spinal cord injury (SCI). The complex pathological factors of diabetes increase the difficulty of treating diabetes combined with SCI. Maintaining normal microglial function is essential for SCI recovery. However, it is unclear whether diabetes hinders nerve recovery after SCI by influencing normal microglial function. This study explored the role and regulatory mechanism of diabetes in microglial function during SCI recovery. We constructed a type 2 diabetes (T2D) combined with SCI mouse model and confirmed that T2D hinders nerve repair after SCI. T2D blocked phagocytizing function of microglia in SCI mice, which results in increased myelin debris accumulation and poor remyelination. A mechanistic study demonstrated that T2D triggers activation of NLRP3 inflammasome by activating the RAGE-ROS-TXNIP axis and then induces excessive microglial pyroptosis, which consequently leads to considerable loss of microglia after SCI. Verapamil (VRP; a TXNIP inhibitor) treatment confirmed that TXNIP is necessary for NLRP3 inflammasome activation. Conditional microglial
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