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首页> 外文期刊>Current drug targets. CNS and neurological disorders >The Nrf2-ARE Signalling pathway: promising drug target to combat oxidative stress in neurodegenerative disorders.
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The Nrf2-ARE Signalling pathway: promising drug target to combat oxidative stress in neurodegenerative disorders.

机译：Nrf2-ARE信号传导途径：有望在神经退行性疾病中对抗氧化应激的药物靶标。

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A large body of evidence indicates that oxidative stress is a salient pathological feature in many neurodegenerative diseases, including Amyotrophic lateral sclerosis, Alzheimer's disease, and Parkinson's disease. In addition to signs of systemic oxidative stress, at the biochemical and neuropathological level, neuronal degeneration in these disorders has been shown to coincide with several markers of oxidative damage to lipids, nucleic acids, and proteins in affected brain regions. Neuroinflammatory processes, often associated with the induction of free radical generating enzymes and the accumulation of reactive astrocytes and microglial cells, are considered as a major source of oxidative stress. Given the pathogenic impact of oxidative stress and neuroinflammation, therapeutic strategies aimed to blunt these processes are considered an effective way to confer neuroprotection. Recently, the nuclear transcription factor Nrf2, that binds to the antioxidant response element (ARE) in gene promoters, has been reported to constitute a key regulatory factor in the co-ordinate induction of a battery of endogenous cytoprotective genes, including those encoding for both antioxidant- and anti-inflammatory proteins. In the present review, besides discussing recent evidence underscoring the thesis that the Nrf2-ARE signalling pathway is an attractive therapeutic target for neurodegenerative diseases, we advocate the view that chemopreventive agents might be suitable candidates to serve as lead compounds for the development of a new class of neuroprotective drugs.
机译：大量证据表明，氧化应激是许多神经退行性疾病（包括肌萎缩性侧索硬化症，阿尔茨海默氏病和帕金森氏病）的主要病理特征。除了系统性氧化应激的迹象外，在生化和神经病理学水平上，这些疾病中的神经元变性还显示出与受影响的大脑区域中脂质，核酸和蛋白质的氧化损伤的几种标志物相吻合。神经炎性过程通常与自由基产生酶的诱导以及反应性星形胶质细胞和小胶质细胞的积累有关，被认为是氧化应激的主要来源。考虑到氧化应激和神经炎症的致病作用，旨在钝化这些过程的治疗策略被认为是赋予神经保护作用的有效方法。最近，据报道，与基因启动子中的抗氧化反应元件（ARE）结合的核转录因子Nrf2构成了协调诱导一系列内源性细胞保护性基因（包括编码这两个基因的基因）的关键调控因子。抗氧化剂和抗炎蛋白。在本综述中，除了讨论最近的证据强调Nrf2-ARE信号通路是神经退行性疾病的诱人治疗靶点这一论点外，我们提倡化学预防剂可能适合作为新化合物开发的先导化合物的观点。一类神经保护药。

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