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Immunometabolic Reprogramming in Experimental Sepsis: A Driver of Multiple Organ Dysfunction Syndrome
Fan Wu1, Yantong Chen1, Lihua Chen2
1Special Education College, Beijing Union University, Beijing, People's Republic of China.
Journal of Inflammation Research
|March 10, 2026
Summary
Sepsis triggers immunometabolic reprogramming, altering cell metabolism and leading to organ damage. Understanding these metabolic shifts is key to developing new sepsis treatments.
Area of Science:
- Immunology
- Metabolism
- Pathophysiology
Background:
- Sepsis is a life-threatening condition with high mortality, driven by systemic inflammation and immune dysregulation.
- Immunometabolic reprogramming is a critical factor in sepsis progression and organ injury.
- Multiple organ dysfunction syndrome (MODS) is a common, fatal outcome of sepsis.
Purpose of the Study:
- To systematically review metabolic alterations in immune cells and organs during experimental sepsis.
- To examine the role of immunometabolism in sepsis-induced organ damage and MODS.
- To identify potential therapeutic targets based on metabolic dysfunctions.
Main Methods:
- Systematic review of experimental sepsis models.
- Analysis of metabolic changes in immune cells and organs.
- Examination of temporal progression of pathological and metabolic changes.
Main Results:
- Key metabolic alterations include enhanced glycolysis, impaired mitochondrial function, and disturbed lipid metabolism.
- These metabolic changes are linked to organ damage, immune response modulation, and MODS development.
- Organ-specific metabolic dysfunctions and inter-organ crosstalk are significant in sepsis.
Conclusions:
- Dynamic immunometabolic regulation and tissue-specific responses are crucial for sepsis treatment.
- Integrating multi-omics, biomarkers, and personalized strategies can advance clinical translation.
- Targeting metabolic pathways offers potential for novel sepsis therapies.
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