Research Progress of Glucose Metabolism Reprogramming in Endometriosis

doi:10.12280/gjfckx.20230069

Abstract

Abstract:

Endometriosis is a chronic inflammatory disease characterized by pain and infertility as the main clinical manifestations. It seriously affects the physical and mental health of women of reproductive age and requires long-term management. So far, there is no effective way to cure this disease. At present, several studies have confirmed that the existence of glucose metabolism reprogramming in endometriosis, where high glucose intake provides the raw material for energy metabolism. The increased expression level of glycolysis-related enzymes realizes the transformation of cell metabolism from aerobic oxidation to glycolysis, resulting in the accumulation of lactic acid and promoting the progress of endometriosis. The regulation of glucose metabolism reprogramming is not fully understood and is mostly related to the hypoxic microenvironment. This shift in metabolic patterns is crucial for cell survival and disease progression. It can be seen that targeting glucose, lactate transporters, glucose metabolism-related enzymes and regulatory factors can provide useful support for patients with endometriosis.

Key words: Endometriosis, Glucose metabolism reprogramming, Glycolysis, Warburg effect, Drug therapy

LI Shang-jin, ZHANG Bing, CONG Shan-shan, ZHAO Shao-jie. Research Progress of Glucose Metabolism Reprogramming in Endometriosis[J]. Journal of International Obstetrics and Gynecology, 2023, 50(3): 246-250.

Figures/Tables 2

References 39

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药物	靶点	机制
抑制葡萄糖摄取与乳酸转运
阿托伐他汀和白藜芦醇	GLUT1和GLUT3	抑制糖酵解和新生血管形成^[25]
桂芝福灵胶囊	GLUT4	抑制高糖的摄入^[26]
AZD0095	MCT4	抑制乳酸的堆积^[27]（肿瘤中应用，EMs中未研究）
抑制糖代谢相关酶
3-溴丙酮酸	HK2	抑制糖酵解，减少子宫内膜间质细胞的迁移和增殖^[6]
PFKFB3抑制剂	PKM2	抑制糖酵解，调节线粒体功能^[28]
二氯乙酸盐（dichloroacetate，DCA）	PDK和PDH	涉及机制多，有前景，见下文详述
苏木心材	PDK1	抑制糖酵解；增加活性氧、下调膜电位致异位子宫内膜细胞凋亡^[29]
糖酵解相关调控因子
2-甲氧基雌二醇	HIF-1α	抑制HIF-1α下游蛋白，如GLUT1^[30]
芍药醇	HIF-1α	抑制HIF-1α诱导的病变^[31]
姜黄素	HIF通路	改善缺氧、降低炎症，下调HIF-1α表达^[32]
KRIBB11	HSF1	调控PFKFB3从而抑制糖酵解^[23]
YL-109	hsc70互作蛋白	hsc70互作蛋白诱导高迁移率族蛋白1泛素化和降解，抑制糖酵解^[33]

药物	靶点	机制
抑制葡萄糖摄取与乳酸转运
阿托伐他汀和白藜芦醇	GLUT1和GLUT3	抑制糖酵解和新生血管形成^[25]
桂芝福灵胶囊	GLUT4	抑制高糖的摄入^[26]
AZD0095	MCT4	抑制乳酸的堆积^[27]（肿瘤中应用，EMs中未研究）
抑制糖代谢相关酶
3-溴丙酮酸	HK2	抑制糖酵解，减少子宫内膜间质细胞的迁移和增殖^[6]
PFKFB3抑制剂	PKM2	抑制糖酵解，调节线粒体功能^[28]
二氯乙酸盐（dichloroacetate，DCA）	PDK和PDH	涉及机制多，有前景，见下文详述
苏木心材	PDK1	抑制糖酵解；增加活性氧、下调膜电位致异位子宫内膜细胞凋亡^[29]
糖酵解相关调控因子
2-甲氧基雌二醇	HIF-1α	抑制HIF-1α下游蛋白，如GLUT1^[30]
芍药醇	HIF-1α	抑制HIF-1α诱导的病变^[31]
姜黄素	HIF通路	改善缺氧、降低炎症，下调HIF-1α表达^[32]
KRIBB11	HSF1	调控PFKFB3从而抑制糖酵解^[23]
YL-109	hsc70互作蛋白	hsc70互作蛋白诱导高迁移率族蛋白1泛素化和降解，抑制糖酵解^[33]