期刊
REVIEWS IN THE NEUROSCIENCES
卷 29, 期 5, 页码 547-555出版社
WALTER DE GRUYTER GMBH
DOI: 10.1515/revneuro-2017-0075
关键词
aerobic glycolysis; amyotrophic lateral disease; Huntington's disease; Warburg effect; WNT/beta-catenin pathway
Neurodegenerative cells are the sites of numerous metabolic and energetic abnormalities with abnormalities in energy production. Energy is the primary determinant of neuronal viability. In neurodegenerative cells, metabolic enzymes are modified by the dysregulation of the canonical WNT/beta-catenin pathway. In amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD), WNT/beta-catenin pathway is upregulated. We focused this review on the hypothesis of aerobic glycolysis stimulated by the upregulation of WNT/beta-catenin pathway in ALS and HD. Upregulation of WNT/beta-catenin pathway induces aerobic glycolysis, named Warburg effect, through activation of glucose transporter (Glut), pyruvate kinase M2 (PKM2), pyruvate dehydrogenase kinase 1 (PDK1), monocarboxylate lactate transporter 1 (MCT-1), lactate dehydrogenase kinase-A (LDH-A), and inactivation of pyruvate dehydrogenase complex (PDH). Aerobic glycolysis consists of a supply of a large part of glucose into lactate regardless of oxygen. Aerobic glycolysis is less efficient in terms of ATP production compared with oxidative phosphorylation because of the shunt of the TCA cycle. Dysregulation of energetic metabolism promotes cell death and disease progression in ALD and HD. Aerobic glycolysis regulation is an attractive mechanism for developing therapeutic interventions.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据