# Decoding Epigenetic Switches: How Histone Acetylation/Deacetylation Regulates Mononuclear/Macrophage Fate in Bone Disorders

## TL;DR

This paper reviews how histone acetylation and deacetylation control macrophage behavior and bone disorders.

## Contribution

The paper systematically examines the epigenetic regulation of macrophage fate in bone diseases.

## Key findings

- Histone acetylation and deacetylation regulate macrophage gene expression and polarization.
- These epigenetic changes influence osteoclast differentiation and pathological bone remodeling.
- The epigenetic network has translational potential for treating bone-related diseases.

## Abstract

Monocyte-macrophage plays a central role in innate immunity, tissue homeostasis maintenance, and disease progression. These phagocytes, which originate from blood monocytes or embryonic sources, are imperative for inflammatory responses, tissue repair, and bone remodeling. In orthopedic diseases, including osteoarthritis, rheumatoid arthritis, osteoporosis, and fractures, changes in histone acetylation are key to regulating macrophage gene expression, polarization, differentiation into osteoclasts, and pathological bone remodeling. Histone acetylation (mediated by histone acetylases) and deacetylation (mediated by histone deacetylases) directly influence important transcription factors in the monocyte-macrophage system by dynamically modulating chromatin accessibility. This review systematically examines the epigenetic network involving histone acetylation and deacetylation monocyte-macrophage, exploring its translational potential in bone-related diseases.