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氧化应激和 Nrf2 在糖尿病性神经病发病机制中的作用:旧观点,新视角。

Oxidative stress and Nrf2 in the pathophysiology of diabetic neuropathy: old perspective with a new angle.

机构信息

Molecular Neuropharmacology Laboratory, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Punjab, India.

出版信息

Biochem Biophys Res Commun. 2011 Apr 29;408(1):1-5. doi: 10.1016/j.bbrc.2011.03.087. Epub 2011 Mar 31.

Abstract

Long-standing diabetes and complications thereof particularly, neuropathy stands for one of the major causes of morbidity across the globe. It is postulated that excessive production of reactive oxygen species is a key component in the development and progression of diabetic neuropathy. Oxidative damage is the most common concluding pathway for various pathogenetic mechanisms of neuronal injury in diabetic neuropathy. However despite optimistic preclinical data, it is still very ambiguous that why antioxidants have failed to demonstrate significant neuroprotection in humans. A growing body of evidences now suggests that strategies utilizing a more targeted approach like focusing on Nrf2 (a transcription factor modulating oxidative stress) may provide an enthralling avenue to optimize neuroprotection in diabetes and diabetic neuropathy. This review presents an emerging concept of Nrf2 in diabetic neuropathy; thus looking forward to newer strategies for combating the oxidant induced damage.

摘要

长期存在的糖尿病及其并发症,尤其是神经病变,是全球发病率的主要原因之一。据推测,活性氧的过度产生是糖尿病性神经病发展和进展的关键组成部分。氧化损伤是糖尿病性神经病中神经元损伤各种发病机制的最常见的终末途径。然而,尽管有乐观的临床前数据,但抗氧化剂为何未能在人类中显示出显著的神经保护作用仍非常不明确。越来越多的证据表明,利用更具针对性的策略的策略,如专注于 Nrf2(一种调节氧化应激的转录因子),可能为优化糖尿病和糖尿病性神经病中的神经保护提供一个诱人的途径。本综述介绍了 Nrf2 在糖尿病性神经病中的新兴概念,因此期待着针对氧化剂诱导损伤的新策略。

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