Interaction Networks Of Macrophage Glycolysis And Inflammation In Sepsis: Mechanisms And Therape

08 Apr 20264 min read0 viewsJournal Feed

GIST

Sepsis is a severe threat to human health with high mortality rates, but so far its pathogenesis is unclear and lacks effective therapeutic drugs. Macrophages function as one of the most important innate immune cells and play an integral role in the sepsis inflammatory process.

Recently, studies have shown that its immune function is associated with the Warburg effect. The Warburg effect refers to the preferential metabolism of glucose to lactate by cells through aerobic glycolysis even with abundant oxygen.

It has shown that increasing aerobic glycolysis promotes M1 polarization of macrophages to facilitate inflammation, whereas decreasing aerobic glycolysis can lead to M2 polarization and alleviated inflammation. Interestingly, it was demonstrated that not only does glycolysis affect inflammation, but inflammation in sepsis in turn affects glycolysis.

Currently, there is no comprehensive review regarding this issue. Therefore, our review focuses on the mechanisms of the interaction between inflammation and macrophage glycolysis in sepsis.

We will address both how inflammatory molecules affect the process of glycolysis in septic macrophages and how glycolytic enzymes and related metabolites contribute to inflammation.

Clinical Editorial

Context and scope

It also considers the therapeutic promise of targeting glycolysis in sepsis.

The source outlines sepsis as a condition with high mortality and unclear pathogenesis, noting macrophages as pivotal innate immune players in sepsis-driven inflammation.
A central theme is the Warburg effect: cells preferentially convert glucose to lactate via aerobic glycolysis despite adequate oxygen, linking energy metabolism to immune function.
The review aims to synthesize how inflammatory signals influence glycolysis in septic macrophages and, conversely, how glycolytic enzymes and metabolites shape inflammatory responses.

Study design and evidence context

The content is presented as a narrative synthesis of mechanistic relationships between macrophage metabolism and inflammation in sepsis, rather than a primary experimental report.
It emphasizes bidirectional interactions: inflammatory mediators modulating glycolytic flux and glycolytic pathways feeding back to regulate macrophage polarization and inflammatory outcomes.

Population, exposure, and intervention landscape

oxidative metabolism) influences M1 versus M2 polarization and inflammatory tone.

Macrophages are highlighted as the primary cell type of interest, with attention to how their metabolic state (aerobic glycolysis vs.
The discussion includes enzymes and metabolites linked to glycolysis as contributors to inflammatory processes, implying potential metabolic targets for intervention.

Limitations and practical relevance

The summary explicitly notes the absence of a comprehensive prior review on this specific interaction in sepsis, signaling the novelty and potential gaps in consolidated evidence.