Lipopolysaccharide-induced glycolytic reprogramming drives H3K18 lactylation-mediated inflammatory injury in buffalo mammary epithelial cells.
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Abstract
reduced lactate accumulation, decreased H3K18la levels, and substantially attenuated inflammatory injury in BuMECs. Together, these findings identify the HK2-lactate-H3K18la axis as a central mechanism in LPS-induced inflammatory injury in BuMECs and underscore its potential as a therapeutic target for alleviating mastitis and enhancing mammary health in dairy buffalo.
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Authors: Peng Xiao, Tian Xin-Ru, Zhou Jin-chen, Bo Zhang, Meng-qi Li, Chunyan Yang, Haiying Zheng, Chen Meng-Jiao, Xiaogan Yang, Jiang-Hua Shang, Xingwei Liang
Institutions: Guangxi University, Guangxi Buffalo Research Institute