Atopic dermatitis: diagnosis, molecular pathogenesis, and therapeutics.

IF 10.1 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Ruimin Bai, Yan Zheng, Xiaofeng Dai
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Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by acute and chronic phases with no definitive cure currently available. The diagnosis of AD involves the evaluation of both disease onset and severity, relying on established clinical criteria and, increasingly, on various biomarkers to improve diagnostic accuracy. The molecular pathogenesis of AD is driven by a combination of genetic predispositions, environmental factors, and immune dysregulation. Acute AD is predominantly mediated by T-helper cell 2 (Th2) immune responses, whereas chronic AD involves a shift toward Th1-driven inflammation. Within this immunological context, we emphasize the role of redox imbalance in disease progression and propose a wound-healing model to explain the molecular dynamics of AD. According to this model, the acute phase is marked by excessive oxidative stress, requiring antioxidant intervention, whereas the chronic phase is characterized by insufficient redox signaling, which hinders the clearance of hyperproliferative cells. We further review current and emerging therapeutic strategies, including anti- and pro-oxidative strategies, based on the different AD staging. Notably, we introduced cold atmospheric plasma (CAP), a redox regulatory tool, as a novel treatment modality for AD management that stimulates antioxidant responses at low to moderate doses and induces oxidative stress at higher concentrations, potentially reversing chronic AD pathology. This review offers a comprehensive overview of AD, from clinical manifestations and molecular pathogenesis to therapeutic approaches, and introduces the 'wound healing model' as a conceptual framework to integrate CAP as an innovative treatment modality for AD management and to inform future research.

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特应性皮炎:诊断、分子发病机制和治疗。
特应性皮炎(AD)是一种慢性炎症性皮肤病,具有急性和慢性期的特征,目前尚无明确的治疗方法。阿尔茨海默病的诊断涉及对疾病发病和严重程度的评估,依赖于既定的临床标准,并越来越多地依赖于各种生物标志物来提高诊断准确性。AD的分子发病机制是由遗传易感性、环境因素和免疫失调共同驱动的。急性AD主要由t辅助细胞2 (Th2)免疫反应介导,而慢性AD则转向th1驱动的炎症。在这种免疫学背景下,我们强调氧化还原失衡在疾病进展中的作用,并提出了一个伤口愈合模型来解释AD的分子动力学。根据该模型,急性期以过度氧化应激为特征,需要抗氧化干预,而慢性期以氧化还原信号不足为特征,阻碍了对超增殖细胞的清除。我们进一步回顾了当前和新兴的治疗策略,包括抗氧化和促氧化策略,基于不同的AD分期。值得注意的是,我们引入了冷大气等离子体(CAP),一种氧化还原调节工具,作为AD管理的一种新型治疗方式,在低至中等剂量下刺激抗氧化反应,在高浓度下诱导氧化应激,可能逆转慢性AD病理。本文综述了从临床表现、分子发病机制到治疗方法的AD的全面概述,并介绍了“伤口愈合模型”作为一个概念框架,将CAP作为AD管理的创新治疗方式,并为未来的研究提供信息。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
6.30
自引率
0.00%
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0
审稿时长
10 weeks
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