ArticleResearch (Washington, D.C.)2025
A Self-Assembled Metabolic Regulator Reprograms Macrophages to Combat Cytokine Storm and Boost Sepsis Immunotherapy.
Article in Research (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The trial behind it
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Who cites it
22 citing papers in PubMed.
- Multi-targeted biomimetic CeO₂-based nanoplatform for sepsis therapy via mitochondrial homeostasis.International journal of pharmaceutics: X · 2026Article
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- The cGAS-STING pathway: mechanistic basis, dual biological functions and translational therapeutic advances.Apoptosis : an international journal on programmed cell death · 2026Review
- A placental and fetal liver TGFβ signaling axis drives fetal immunosuppression in maternal obesity.iScience · 2026Article
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Carrier-Free Nanoassembly Suppresses Phase Separation via Ribosome-Inspired Crowding Control for Enhanced Chemo-Immunotherapy.ACS nano · 2026Article
- From nanotechnology to immunomodulation: emerging strategies targeting macrophages in high altitude pulmonary hypertension.Journal of nanobiotechnology · 2026Review
- Glutathione peroxidase mimic-engineered α-lactalbumin self-assembling coatings tailor immunomodulatory vascular stents for suppressing restenosis.Bioactive materials · 2026Article
- Immunological mechanisms and novel therapeutic strategies for sepsis‑associated acute kidney injury (Review).International journal of molecular medicine · 2026Review
- Targeted inhibition of PARP-1 in pulmonary epithelial cells and macrophages via SPA-functionalized microparticles attenuates sepsis-induced lung injury.Materials today. Bio · 2026Article
- Nanotherapeutic Macrophage-Neuro Reprogramming Through Immunometabolic Crosstalk Mitigates Sepsis-Induced Lung Injury and Neurologic Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Macrophage-Mimicking Biomimetic Microbubbles for Early Ultrasound Molecular Imaging of Acute Rejection in Heart Transplantation.ACS applied materials & interfaces · 2026Article
- Macrophage metabolic reprogramming in sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
- Splenic PD-L1Research (Washington, D.C.) · 2026Article
- Macrophage Hypoxia Signaling Pathways and Their Roles in Sepsis.Journal of inflammation research · 2026Review
- The immunometabolic axis of sepsis-related myocardial injury: macrophage reprogramming as a central mechanism and therapeutic target.Frontiers in immunology · 2026Review
- Mitochondrial immunometabolism in sepsis: orchestrating macrophage polarization and dysfunction.European journal of medical research · 2025Review
- Exploring the role of palmitoylation in sepsis: mechanistic insights and future perspectives.Molecular medicine (Cambridge, Mass.) · 2025Review
- Targeting Matrix Metalloproteinase-9 to Alleviate T Cell Exhaustion and Improve Sepsis Prognosis.Research (Washington, D.C.) · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
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 derivative with the glycolysis inhibitor Lonidamine. By concurrently targeting glycolysis and STING pathways, LDO reprograms macrophages to restore balanced polarization. In sepsis models, LDO effectively attenuates CCL2-driven cytokine storms, alleviates acute lung injury, and significantly enhances survival via metabolic reprogramming. This study offers a cytokine-regulatory strategy rooted in immunometabolism, providing a foundation for the translational development of immune metabolite-based sepsis therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.