# Lactylation modification - a bridge between sepsis and macrophage metabolic reprogramming

## TL;DR

This paper explores how lactylation, an epigenetic modification, connects sepsis with changes in macrophage metabolism and inflammation.

## Contribution

The paper highlights lactylation as a novel mechanism linking sepsis and macrophage metabolic reprogramming.

## Key findings

- Lactate acts as a key regulator through histone lactylation in macrophages during sepsis.
- Lactylation fine-tunes macrophage function and corrects inflammatory imbalances.
- The review provides insights into lactylation's role in sepsis-related metabolic control.

## Abstract

Sepsis is a life-threatening organ failure syndrome triggered by dysregulated host responses to infection. During disease progression, macrophages drive initial hyperinflammatory responses and critically regulate the subsequent immunosuppressive phase. Emerging evidence reveals that macrophage phenotypes dynamically adapt through metabolic reprogramming, creating phenotype-metabolism interdependence. Notably, lactate—long considered merely a glycolytic byproduct—now emerges as a key regulator through histone lactylation. This epigenetic modification fine-tunes macrophage functionality and corrects inflammatory imbalance in sepsis. This breakthrough illuminates lactylation’s central role in macrophage regulation, opening new diagnostic and therapeutic avenues. This review comprehensively examines lactylation mechanisms and their impact on metabolic control in sepsis-associated macrophages.