Lipopolysaccharide-induced glycolytic reprogramming drives H3K18 lactylation-mediated inflammatory injury in buffalo mammary epithelial cells.
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.
Authors
- Meng-qi Li
- Jiang-Hua Shang
- Xiaogan Yang (ORCID: https://orcid.org/0000-0002-7431-8914)
- Haiying Zheng (ORCID: https://orcid.org/0000-0001-9050-5309)
- Xingwei Liang (ORCID: https://orcid.org/0000-0002-7419-8617)
- Zhou Jin-chen
- Chunyan Yang (ORCID: https://orcid.org/0009-0007-6957-647X)
- Tian Xin-Ru
- Chen Meng-Jiao
- Peng Xiao
- Bo Zhang
Institutions
- Guangxi University (CN)
- Guangxi Buffalo Research Institute (CN)
Publication Details
- Journal
- PubMed
- Published
- 2026-09-18
- DOI
- https://doi.org/10.24272/j.issn.2095-8137.2025.523
- Primary Topic
- Milk Quality and Mastitis in Dairy Cows
- Type
- article
- Field-Weighted Citation Impact
- 0.00