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特应性皮炎与丝聚合蛋白。

Atopic dermatitis and filaggrin.

机构信息

Department of Dermatology and Allergy, University of Bonn, Sigmund-Freud-Str., 25, 53127 Bonn, Germany.

Department of Dermatology and Allergy, University of Bonn, Sigmund-Freud-Str., 25, 53127 Bonn, Germany.

出版信息

Curr Opin Immunol. 2016 Oct;42:1-8. doi: 10.1016/j.coi.2016.05.002. Epub 2016 May 17.

Abstract

Filaggrin has a key structural and functional role in the epidermis with important impact on the homeostasis of the skin. Inherited or acquired filaggrin deficiency has been described to essentially contribute to the pathogenesis of atopic dermatitis (AD), one of the most frequent chronic eczematous skin diseases in child-hood and adult-hood. Increasing knowledge has been gained during the last years about direct and indirect consequences of filaggrin deficiency. Furthermore, with the help of novel murine and human experimental models important steps forward have been made towards the characterization of filaggrin structure and function. Future approaches aimed at restoration of filaggrin expression may open novel mechanism-based therapies for AD.

摘要

丝聚合蛋白在表皮中具有关键的结构和功能作用,对皮肤的内稳态有重要影响。遗传或获得性丝聚合蛋白缺乏被认为是特应性皮炎(AD)发病机制的重要因素,AD 是儿童和成人中最常见的慢性湿疹性皮肤病之一。近年来,人们对丝聚合蛋白缺乏的直接和间接后果有了更多的了解。此外,借助新型的小鼠和人类实验模型,丝聚合蛋白结构和功能的特征也取得了重要进展。未来旨在恢复丝聚合蛋白表达的方法可能为 AD 提供新的基于机制的治疗方法。

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