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作 者:Jie Chen Pengfei Qin Yanli Sun Suping Han
机构地区:[1]Department of Obstetrics and Gynecology,Women's Hospital of Nanjing Medical University,Nanjing Maternity and Child Health Care Hospital,Nanjing,Jiangsu 210004,China [2]Department of Gynecology,the First Affiliated Hospital of Nanjing Medical University,Nanjing,Jiangsu 210004,China
出 处:《The Journal of Biomedical Research》2023年第6期470-478,共9页生物医学研究杂志(英文版)
摘 要:Endometriosis is defined as a condition with endometrium-like tissues migrating outside of the pelvic cavity.However,the mechanism of endometriosis is still unclear.Lactate can be covalently modified to lysine residues of histones and other proteins,which is called lactylation.The results showed that the higher level of lactate and lactate dehydrogenase A enhanced the histone H3 lysine 18 lactylation(H3K18lac)in ectopic endometrial tissues and ectopic endometrial stromal cells than that in normal endometrial tissues and normal endometrial stromal cells.Lactate promoted cell proliferation,migration,and invasion in endometriosis.Mechanistically,lactate induced H3K18lac to promote the expression of high-mobility group box 1(HMGB1)in endometriosis,and HMGB1 knockdown significantly reduced the cell proliferation,migration,and invasion of the lactate-treated cells through the phosphorylation of AKT.In conclusion,lactate could induce histone lactylation to promote endometriosis progression by upregulating the expression of HMGB1,which may provide a novel target for the prevention and treatment of endometriosis.
关 键 词:ENDOMETRIOSIS ESCS LACTATE lactylation HMGB1
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