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ALS and Oxidative Stress: The Neurovascular Scenario

机译:ALS和氧化应激:神经血管情景

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Oxidative stress and angiogenic factors have been placed as the prime focus of scientific investigations after an establishment of link between vascular endothelial growth factor promoter (VEGF), hypoxia, and amyotrophic lateral sclerosis (ALS) pathogenesis. Deletion of the hypoxia-response element in the vascular endothelial growth factor promoter and mutant superoxide dismutase 1 (SOD1) which are characterised by atrophy and muscle weakness resulted in phenotype resembling human ALS in mice. This results in lower motor neurodegeneration thus establishing an important link between motor neuron degeneration, vasculature, and angiogenic molecules. In this review, we have presented human, animal, andin vitrostudies which suggest that molecules likeVEGFhave a therapeutic, diagnostic, and prognostic potential in ALS. Involvement of vascular growth factors and hypoxia response elements also highlights the converging role of oxidative stress and neurovascular network for understanding and treatment of various neurodegenerative disorders like ALS.
机译:在建立血管内皮生长因子启动子(VEGF),缺氧和肌萎缩性侧索硬化(ALS)发病机制之间的联系之后,氧化应激和血管生成因子已成为科学研究的主要重点。以萎缩和肌肉无力为特征的血管内皮生长因子启动子和突变型超氧化物歧化酶1(SOD1)中缺氧反应元件的缺失导致小鼠的表型类似于人ALS。这导致较低的运动神经变性,因此在运动神经元变性,脉管系统和血管生成分子之间建立了重要的联系。在这篇综述中,我们介绍了人类,动物和体外研究,这些研究表明像VEGF的分子在ALS中具有治疗,诊断和预后的潜力。血管生长因子和缺氧反应元件的参与还突出了氧化应激和神经血管网络在理解和治疗各种神经退行性疾病(如ALS)中的聚合作用。

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