Histone lactylation at H4K12 promotes macrophage-fibroblast crosstalk in neodymium oxide-induced pulmonary fibrosis via the PIK3R2/PI3K/Akt/mTOR axis

Chemico-Biological Interactions 2026 Open access

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Authors: Wenjie Li, Xi Chen, Y L Zhao, Xin Su, Kai Wu, Yi Zhang, Yanhong Dong, Yanrong Gao, Suhua Wang
DOI: 10.1016/j.cbi.2026.112216
Cited by: 1
References: 63

Abstract

-induced macrophage-fibroblast interactions and elucidate the molecular mechanism underlying the regulation of PIK3R2 expression by H4K12 lactylation. This regulation, in turn, activates the PI3K/Akt/mTOR-signaling pathway and the fibrotic process, thus providing novel potential epigenetic targets for the prevention and treatment of lung fibrosis.

Fields of Study & Subjects

Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis Immune cells in cancer Cardiac Fibrosis and Remodeling

Publication details

Journal / source
Chemico-Biological Interactions
Publisher
Elsevier BV
Volume
436
Pages
112216–112216
Publication date
21 June 2026
Language
EN