# Role of lactylation-induced macrophage failed phenotypic switching in sustaining inflammation of diabetic wounds

## TL;DR

This paper explores how lactylation in macrophages contributes to chronic inflammation in diabetic wounds and suggests targeting lactylation as a potential treatment.

## Contribution

The paper introduces lactylation as a novel regulator of macrophage function in diabetic wound inflammation.

## Key findings

- Lactylation affects macrophage metabolism and polarization in diabetic wounds.
- Chronic inflammation is linked to lactylation-induced macrophage phenotypic switching.
- Targeting lactylation may offer therapeutic benefits for diabetic wound healing.

## Abstract

The impaired healing of diabetic wounds is closely associated with a persistent inflammatory response, wherein macrophages, as crucial immune effector cells in the local wound microenvironment, play a vital role in maintaining inflammatory equilibrium. Increasing evidence indicates that lactate, a product of glycolysis, is now recognized as a novel regulator of macrophage function by influencing gene transcription through protein lactylation on histone and non-histone substrates. This review seeks to outline the impact of chronic inflammation on macrophage phenotype (metabolism and polarization) and to clarify how subsequent protein lactylation alters macrophage biology, thereby impacting the progression of chronic inflammatory conditions such as diabetic wounds. These findings collectively provide new insights into the pathogenesis of impaired diabetic wound healing and underscore the potential of targeting protein lactylation as a therapeutic approach against chronic inflammation.