PDF(Pubmed)
Abstract：
Diabetic neuropathy (DN) is a neurodegenerative disorder that is primarily characterized by distal sensory loss, reduced mobility, and foot ulcers that may potentially lead to amputation. The multifaceted etiology of DN is linked to a range of inflammatory, vascular, metabolic, and other neurodegenerative factors. Chronic inflammation, endothelial dysfunction, and oxidative stress are the three basic biological changes that contribute to the development of DN. Although our understanding of the intricacies of DN has advanced significantly over the past decade, the distinctive mechanisms underlying the condition are still poorly understood, which may be the reason behind the lack of an effective treatment and cure for DN. The present study delivers a comprehensive understanding and highlights the potential role of the several pathways and molecular mechanisms underlying the etiopathogenesis of DN. Moreover, Schwann cells and satellite glial cells, as integral factors in the pathogenesis of DN, have been enlightened. This work will motivate allied research disciplines to gain a better understanding and analysis of the current state of the biomolecular mechanisms behind the pathogenesis of DN, which will be essential to effectively address every facet of DN, from prevention to treatment.
摘要：
糖尿病性神经病（DN）是一种神经退行性疾病，主要表现为远端感觉丧失，流动性降低，和可能导致截肢的足部溃疡。DN的多方面病因与一系列炎症有关，血管,新陈代谢，和其他神经退行性因素。慢性炎症,内皮功能障碍,和氧化应激是促成DN发生发展的三个基本生物学改变。尽管在过去的十年中，我们对DN复杂性的理解有了显著的进步，这种疾病背后的独特机制仍然知之甚少，这可能是缺乏有效治疗和治愈DN的原因。本研究提供了全面的理解，并强调了DN病因的几种途径和分子机制的潜在作用。此外，雪旺氏细胞和卫星胶质细胞，作为DN发病的重要因素,已经开悟了。这项工作将激励相关研究学科更好地理解和分析DN发病机理背后的生物分子机制的现状，这对于有效解决DN的各个方面至关重要，从预防到治疗。
