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Related Experiment Video

Updated: Sep 16, 2025

Inducing Apical Periodontitis in Mice

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

KAT6A Promotes Macrophage Inflammation and Periodontitis.

Shi-Jia Huang¹, Shuo Xu^2,3,4,5,6, Hui-Lin Ye^3,4,5,6

¹Department of Orthodontics & Prosthodontics, The Second Affiliated Hospital Zhejiang University School of Medicine, Hangzhou, China.

Journal of Clinical Periodontology

|July 9, 2025

Summary

This summary is machine-generated.

Macrophage lysine acetyltransferase 6A (KAT6A) is upregulated in periodontitis (PD). Targeting KAT6A in macrophages reduces bone loss and inflammation in PD, indicating its therapeutic potential.

Keywords:

KAT6A acetylation macrophage periodontitis

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Last Updated: Sep 16, 2025

Inducing Apical Periodontitis in Mice

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

Three-dimensional Inflammatory Human Tissue Equivalents of Gingiva

Three-dimensional Inflammatory Human Tissue Equivalents of Gingiva

Published on: April 3, 2018

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

Area of Science:

Immunology
Epigenetics
Periodontal disease research

Background:

Periodontitis (PD) involves epigenetic modification and immunoregulation.
The role of macrophage lysine acetyltransferase 6A (KAT6A) in PD pathogenesis is currently unknown.

Purpose of the Study:

To investigate the function of KAT6A in macrophages within the context of periodontitis.

Main Methods:

Analysis of single-cell RNA sequencing data from PD patients.
Generation of macrophage KAT6A knockout (MK6AKO) mice for PD induction models.
RNA sequencing and Cut&tag techniques to analyze gene expression and epigenetic modifications.

Main Results:

KAT6A was upregulated in macrophages of PD patients.
MK6AKO mice exhibited reduced alveolar bone resorption and attenuated inflammatory gene expression post-PD induction.
MK6AKO macrophages showed downregulated inflammatory pathways, including IL-17, and reduced histone acetylation at key inflammatory gene promoters.

Conclusions:

KAT6A plays a significant role in modulating macrophage phenotype and driving periodontitis progression.
Targeting KAT6A presents a potential therapeutic strategy for periodontitis.