Atopic dermatitis: molecular, cellular, and clinical aspects
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 alteration...
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| Veröffentlicht in: | Molecular biology reports 2022-04, Vol.49 (4), p.3333-3348 |
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| creator | Salimian, Jafar Salehi, Zahra Ahmadi, Ali Emamvirdizadeh, Alireza Davoudi, Seyyed Masoud Karimi, Mehrdad Korani, Mohsen Azimzadeh Jamalkandi, Sadegh |
| description | 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. |
| doi_str_mv | 10.1007/s11033-021-07081-7 |
| format | Article |
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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.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-021-07081-7</identifier><identifier>PMID: 34989960</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Atopic dermatitis ; Biomedical and Life Sciences ; Clinical aspects ; Dermatitis ; Dermatitis, Atopic - genetics ; Dysbacteriosis ; Eczema ; Environmental factors ; Filaggrin ; Genetic Predisposition to Disease ; Histology ; Humans ; Immune response ; Life Sciences ; Lipid bilayers ; Microflora ; Morphology ; Phenotypes ; Review ; Skin ; Skin diseases</subject><ispartof>Molecular biology reports, 2022-04, Vol.49 (4), p.3333-3348</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022</rights><rights>2022. 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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.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Atopic dermatitis</subject><subject>Biomedical and Life Sciences</subject><subject>Clinical aspects</subject><subject>Dermatitis</subject><subject>Dermatitis, Atopic - genetics</subject><subject>Dysbacteriosis</subject><subject>Eczema</subject><subject>Environmental factors</subject><subject>Filaggrin</subject><subject>Genetic Predisposition to Disease</subject><subject>Histology</subject><subject>Humans</subject><subject>Immune response</subject><subject>Life Sciences</subject><subject>Lipid bilayers</subject><subject>Microflora</subject><subject>Morphology</subject><subject>Phenotypes</subject><subject>Review</subject><subject>Skin</subject><subject>Skin diseases</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kD1PwzAQhi0EoqXwBxhQJBYGAnd2nEsQS1XxJVVigdlybBelykexk4F_T0oKSAxM55Mfv371MHaKcIUAdB0QQYgYOMZAkGFMe2yKkkSc5JTtsykIwDjJJE7YUQhrAEiQ5CGbiCTP8jyFKbudd-2mNJF1vtZd2ZXhJqrbypm-0v4yMq6qxpNubGSqsimNriIdNs504ZgdrHQV3Mluztjr_d3L4jFePj88LebL2AiSXWy0AcI8lUIUKw7GDasUhbVAmnRClmzCU23IFpSR4NaJBJ3LMpmmCeVSzNjFmLvx7XvvQqfqMmyr6ca1fVA8ReLEEWlAz_-g67b3zdBuoESOXArIB4qPlPFtCN6t1MaXtfYfCkFt3arRrRrcqi-3aht9tovui9rZnyffMgdAjEAYrpo353___if2EwEEglA</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Salimian, Jafar</creator><creator>Salehi, Zahra</creator><creator>Ahmadi, Ali</creator><creator>Emamvirdizadeh, Alireza</creator><creator>Davoudi, Seyyed Masoud</creator><creator>Karimi, Mehrdad</creator><creator>Korani, Mohsen</creator><creator>Azimzadeh Jamalkandi, Sadegh</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3403-3700</orcidid></search><sort><creationdate>20220401</creationdate><title>Atopic dermatitis: molecular, cellular, and clinical aspects</title><author>Salimian, Jafar ; Salehi, Zahra ; Ahmadi, Ali ; Emamvirdizadeh, Alireza ; Davoudi, Seyyed Masoud ; Karimi, Mehrdad ; Korani, Mohsen ; Azimzadeh Jamalkandi, Sadegh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-cac07196533bf20cec0753bdd07a7a47d7d426ac7db78732de341ee8856647953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Atopic dermatitis</topic><topic>Biomedical and Life Sciences</topic><topic>Clinical aspects</topic><topic>Dermatitis</topic><topic>Dermatitis, Atopic - 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Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Salimian, Jafar</au><au>Salehi, Zahra</au><au>Ahmadi, Ali</au><au>Emamvirdizadeh, Alireza</au><au>Davoudi, Seyyed Masoud</au><au>Karimi, Mehrdad</au><au>Korani, Mohsen</au><au>Azimzadeh Jamalkandi, Sadegh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Atopic dermatitis: molecular, cellular, and clinical aspects</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>49</volume><issue>4</issue><spage>3333</spage><epage>3348</epage><pages>3333-3348</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>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.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>34989960</pmid><doi>10.1007/s11033-021-07081-7</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0003-3403-3700</orcidid></addata></record> |
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| subjects | Animal Anatomy Animal Biochemistry Atopic dermatitis Biomedical and Life Sciences Clinical aspects Dermatitis Dermatitis, Atopic - genetics Dysbacteriosis Eczema Environmental factors Filaggrin Genetic Predisposition to Disease Histology Humans Immune response Life Sciences Lipid bilayers Microflora Morphology Phenotypes Review Skin Skin diseases |
| title | Atopic dermatitis: molecular, cellular, and clinical aspects |
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