Atopic dermatitis: molecular, cellular, and clinical aspects

被引：0

作者：

Jafar Salimian

Zahra Salehi

Ali Ahmadi

Alireza Emamvirdizadeh

Seyyed Masoud Davoudi

Mehrdad Karimi

Mohsen Korani

Sadegh Azimzadeh Jamalkandi

机构：

[1] Baqiyatallah University of Medical Sciences,Chemical Injuries Research Center, Systems Biology and Poisonings Institute

[2] Tehran University of Medical Sciences,Department of Immunology, School of Medicine

[3] Baqiyatallah University of Medical Sciences,Molecular Biology Research Center, Systems Biology and Poisonings Institute

[4] Islamic Azad University,Department of Genetics, Faculty of Bio Sciences, Tehran North Branch

[5] Baqiyatallah University of Medical Sciences,Department of Dermatology

[6] Tehran University of Medical Sciences,Department of Traditional Medicine, School of Persian Medicine

[7] Baqiyatallah University of Medical Sciences,Department of Biochemistry, Faculty of Medicine

[8] Shiraz University of Medical Sciences,Research Center for Traditional Medicine and History of Medicine

来源：

Molecular Biology Reports | 2022年 / 49卷

关键词：

Atopic dermatitis; Signaling; Treatment; Microbiota; Pathophysiology;

D O I：

暂无

中图分类号：

学科分类号：

摘要：

Atopic dermatitis (AD) is a complicated, inflammatory skin disease, which numerous genetic and environmental factors play roles in its development. AD is categorized into different phenotypes and stages, although they are mostly similar in their pathophysiological aspects. Immune response alterations and structural distortions of the skin-barrier layer are evident in AD patients. Genetic makeup, lifestyle, and environment are also significantly involved in contextual factors. Genes involved in AD-susceptibility, including filaggrin and natural moisturizing, cause considerable structural modifications in the skin's lipid bilayer and cornified envelope. Additionally, the skin's decreased integrity and altered structure are accompanied by biochemical changes in the normal skin microflora’s dysbiosis. The dynamic immunological responses, genetic susceptibilities, and structural modifications associated with AD's pathophysiology will be extensively discussed in this review, each according to the latest achievements and findings.

引用

页码：3333 / 3348

页数：15

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