Glucose Metabolic Dysfunction in Neurodegenerative Diseases-New Mechanistic Insights and the Potential of Hypoxia as a Prospective Therapy Targeting Metabolic Reprogramming.

Glucose Metabolic Dysfunction in Neurodegenerative Diseases-New Mechanistic Insights and the Potential of Hypoxia as a Prospective Therapy Targeting Metabolic Reprogramming.
复制标题

神经退行性疾病中的葡萄糖代谢功能障碍-新的机制见解和缺氧作为靶向代谢重编程的前瞻性治疗的潜力。

DOI:
10.3390/ijms22115887
复制
发表时间:
2021-05-31
影响因子:
5.6
通讯作者:
Zhou B
Zhou B
中科院分区:
生物学2区
文献类型:
--
作者:
Han R;Liang J;Zhou B

文献摘要

参考文献

被引文献

相似文献

葡萄糖是成人大脑的主要循环能量基质。由于神经细胞的高能量需求,葡萄糖被主动氧化以产生ATP,并且在代谢途径中与线粒体具有协同作用。葡萄糖代谢障碍不可避免地干扰神经元的正常功能,这在神经退行性疾病中被广泛观察到。了解疾病进展过程中的代谢适应机制已成为研究的主要焦点,对这些过程的干预可能会减轻神经元的退行性应激。在这篇综述中,我们强调线粒体功能障碍,葡萄糖摄取减少,减少葡萄糖代谢在不同的神经退行性疾病模型,如阿尔茨海默氏病(AD),帕金森氏病(PD),肌萎缩侧索硬化症(ALS),和亨廷顿病(HD)的证据。我们还讨论了如何缺氧,与肿瘤细胞和正常脑细胞中的葡萄糖代谢代谢的代谢重编程策略,并总结了缺氧作为一般神经退行性疾病的假定治疗的证据。
Glucose is the main circulating energy substrate for the adult brain. Owing to the high energy demand of nerve cells, glucose is actively oxidized to produce ATP and has a synergistic effect with mitochondria in metabolic pathways. The dysfunction of glucose metabolism inevitably disturbs the normal functioning of neurons, which is widely observed in neurodegenerative disease. Understanding the mechanisms of metabolic adaptation during disease progression has become a major focus of research, and interventions in these processes may relieve the neurons from degenerative stress. In this review, we highlight evidence of mitochondrial dysfunction, decreased glucose uptake, and diminished glucose metabolism in different neurodegeneration models such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD). We also discuss how hypoxia, a metabolic reprogramming strategy linked to glucose metabolism in tumor cells and normal brain cells, and summarize the evidence for hypoxia as a putative therapy for general neurodegenerative disease.
GLUT4 动员支持活跃突触的能量需求。
DOI: 10.1016/j.neuron.2016.12.020
发表时间: 2017-02-08
期刊: Neuron
影响因子: 16.2
作者:
Ashrafi G;Wu Z;Farrell RJ;Ryan TA
通讯作者: Ryan TA
DOI: 10.1006/nbdi.1998.0168
发表时间: 1998-04-01
影响因子: 6.1
作者:
Becher, MW;Kotzuk, JA;Ross, CA
通讯作者: Ross, CA
DOI: 10.1111/j.1749-6632.2000.tb06370.x
发表时间: 2000-01-01
期刊: VASCULAR FACTORS IN ALZHEIMER'S DISEASE
影响因子: --
作者:
Blass, JP;Sheu, RKF;Gibson, GE
通讯作者: Gibson, GE
DOI: 10.1016/s0022-510x(01)00627-x
发表时间: 2001-10-15
影响因子: 4.4
作者:
Bendotti, C;Calvaresi, N;De Biasi, S
通讯作者: De Biasi, S
DOI: 10.1007/bf00691318
发表时间: 1981-01-01
影响因子: 12.7
作者:
ATSUMI, T
通讯作者: ATSUMI, T