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了解糖尿病神经病变:关注氧化应激。

Understanding Diabetic Neuropathy: Focus on Oxidative Stress.

机构信息

Department of Anesthesiology, The First Hospital of Jilin University, Jilin, China.

Department of Urology, The First Hospital of Jilin University, Jilin, China.

出版信息

Oxid Med Cell Longev. 2020 Jul 31;2020:9524635. doi: 10.1155/2020/9524635. eCollection 2020.

Abstract

Diabetic neuropathy is one of the clinical syndromes characterized by pain and substantial morbidity primarily due to a lesion of the . The burden of diabetic neuropathy is related not only to the complexity of diabetes but also to the poor outcomes and difficult treatment options. There is no specific treatment for diabetic neuropathy other than glycemic control and diligent foot care. Although various metabolic pathways are impaired in diabetic neuropathy, enhanced cellular oxidative stress is proposed as a common initiator. A mechanism-based treatment of diabetic neuropathy is challenging; a better understanding of the pathophysiology of diabetic neuropathy will help to develop strategies for the new and correct diagnostic procedures and personalized interventions. Thus, we review the current knowledge of the pathophysiology in diabetic neuropathy. We focus on discussing how the defects in metabolic and vascular pathways converge to enhance oxidative stress and how they produce the onset and progression of nerve injury present in diabetic neuropathy. We discuss if the mechanisms underlying neuropathy are similarly operated in type I and type II diabetes and the progression of antioxidants in treating diabetic neuropathy.

摘要

糖尿病性神经病是一种以疼痛为特征的临床综合征,其发病率高,主要是由于 的病变。糖尿病性神经病的负担不仅与糖尿病的复杂性有关,还与不良结局和治疗选择困难有关。除了血糖控制和足部护理外,糖尿病性神经病没有其他特定的治疗方法。虽然糖尿病性神经病中各种代谢途径受损,但增强的细胞氧化应激被认为是一个共同的启动因素。基于机制的糖尿病性神经病治疗具有挑战性;更好地了解糖尿病性神经病的病理生理学将有助于制定新的正确诊断程序和个性化干预策略。因此,我们回顾了糖尿病性神经病的病理生理学的现有知识。我们重点讨论代谢和血管途径的缺陷如何汇集以增强氧化应激,以及它们如何产生糖尿病性神经病中存在的神经损伤的发作和进展。我们讨论了神经病的机制是否在 1 型和 2 型糖尿病中同样起作用,以及抗氧化剂在治疗糖尿病性神经病中的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13ee/7422494/4c656e24e147/OMCL2020-9524635.001.jpg

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