糖酵解
厌氧糖酵解
巴基斯坦卢比
癌症研究
丙酮酸激酶
血管生成
转移
癌症
非酒精性脂肪肝
医学
脂肪肝
生物
疾病
病理
内科学
新陈代谢
作者
Hengdong Qu,Junli Liu,Di Zhang,Ruoyun Xie,Lijuan Wang,Chongqing Gao
出处
期刊:Cells
[MDPI AG]
日期:2023-07-26
卷期号:12 (15): 1930-1930
标识
DOI:10.3390/cells12151930
摘要
Chronic liver diseases (CLDs) cover a spectrum of liver diseases, ranging from nonalcoholic fatty liver disease to liver cancer, representing a growing epidemic worldwide with high unmet medical needs. Glycolysis is a conservative and rigorous process that converts glucose into pyruvate and sustains cells with the energy and intermediate products required for diverse biological activities. However, abnormalities in glycolytic flux during CLD development accelerate the disease progression. Aerobic glycolysis is a hallmark of liver cancer and is responsible for a broad range of oncogenic functions including proliferation, invasion, metastasis, angiogenesis, immune escape, and drug resistance. Recently, the non-neoplastic role of aerobic glycolysis in immune activation and inflammatory disorders, especially CLD, has attracted increasing attention. Several key mediators of aerobic glycolysis, including HIF-1α and pyruvate kinase M2 (PKM2), are upregulated during steatohepatitis and liver fibrosis. The pharmacological inhibition or ablation of PKM2 effectively attenuates hepatic inflammation and CLD progression. In this review, we particularly focused on the glycolytic and non-glycolytic roles of PKM2 in the progression of CLD, highlighting the translational potential of a glycolysis-centric therapeutic approach in combating CLD.
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