{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhuang J"],"funding":["Shaanxi Youth Rising Stars in Science and Technology","Key Research and Development Program of Shaanxi Province","Shaanxi Province Key Industry Innovation Chain Project","National Natural Science Foundation of China","Innovation Capability Support Program of Shaanxi","Shenzhen Science and Technology Program"],"pagination":["0663"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11959697"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8"],"pubmed_abstract":["Sepsis, a life-threatening inflammatory disorder characterized by multiorgan failure, arises from a dysregulated immune response to infection. Modulating macrophage polarization has emerged as a promising strategy to control sepsis-associated inflammation. The endogenous metabolite itaconate has shown anti-inflammatory potential by suppressing the stimulator of interferon genes (STING) pathway, but its efficacy is inhibited by hyperactive glycolysis, which sustains macrophage overactivation. Here, we revealed a critical crosstalk between the itaconate-STING axis and glycolysis in macrophage-mediated inflammation. Building on this interplay, we developed a novel nanoparticle LDO (lonidamine disulfide 4-octyl-itaconate), a self-assembled metabolic regulator integrating an itaconate derivativ"],"journal":["Research (Washington, D.C.)"],"pubmed_title":["A Self-Assembled Metabolic Regulator Reprograms Macrophages to Combat Cytokine Storm and Boost Sepsis Immunotherapy."],"pmcid":["PMC11959697"],"funding_grant_id":["2023-ZDLSF-59","2022SF-374","JCYJ20240813150807010","82173682","2021KJXX-92","2024ZC-KJXX-119"],"pubmed_authors":["Yang L","Lu X","Sun B","Hai Y","Fan R","Zhao M","Han B","Luo L","Wang W","Wei G","Zhang C","Zhang B","Zhuang J"],"additional_accession":[]},"is_claimable":false,"name":"A Self-Assembled Metabolic Regulator Reprograms Macrophages to Combat Cytokine Storm and Boost Sepsis Immunotherapy.","description":"Sepsis, a life-threatening inflammatory disorder characterized by multiorgan failure, arises from a dysregulated immune response to infection. Modulating macrophage polarization has emerged as a promising strategy to control sepsis-associated inflammation. The endogenous metabolite itaconate has shown anti-inflammatory potential by suppressing the stimulator of interferon genes (STING) pathway, but its efficacy is inhibited by hyperactive glycolysis, which sustains macrophage overactivation. Here, we revealed a critical crosstalk between the itaconate-STING axis and glycolysis in macrophage-mediated inflammation. Building on this interplay, we developed a novel nanoparticle LDO (lonidamine disulfide 4-octyl-itaconate), a self-assembled metabolic regulator integrating an itaconate derivativ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-04-08T19:47:18.284Z","creation":"2026-04-08T14:29:05.649Z"},"accession":"S-EPMC11959697","cross_references":{"pubmed":["40171016"],"doi":["10.34133/research.0663"]}}