Keloids: The paradigm of skin fibrosis — Pathomechanisms and treatment
Keloids, fibroproliferative dermal tumors with effusive accumulation of extracellular matrix (ECM) components, particularly collagen, result from excessive expression of growth factors and cytokines. The etiology of keloids is unknown but they occur after dermal injury in genetically susceptible ind...
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Veröffentlicht in: | Matrix biology 2016-04, Vol.51, p.37-46 |
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description | Keloids, fibroproliferative dermal tumors with effusive accumulation of extracellular matrix (ECM) components, particularly collagen, result from excessive expression of growth factors and cytokines. The etiology of keloids is unknown but they occur after dermal injury in genetically susceptible individuals, and they cause both physical and psychological distress for the affected individuals. Several treatment methods for keloids exist, including the combination therapy of surgical excision followed by intralesional steroid therapy, however, they have high recurrence rate regardless of the current treatment method. Improved understanding of the pathomechanisms leading to keloid formation will hopefully identify pathways that serve as specific targets to improve therapy for this devastating, currently intractable, disorder.
•Keloids are dermal tumors characterized by excessive accumulation of collagen.•The key cell responsible for matrix production is activated myofibroblast.•A number of growth factors, particularly TGF-β, play a role in excessive collagen production.•Recent studies have supported a role for Fibronectin Extra Domain A (Fn-EDA) which is markedly upregulated in keloids.•Identification of pathways involved in matrix accumulation allows development of targeted therapies for fibrotic diseases. |
doi_str_mv | 10.1016/j.matbio.2016.01.013 |
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•Keloids are dermal tumors characterized by excessive accumulation of collagen.•The key cell responsible for matrix production is activated myofibroblast.•A number of growth factors, particularly TGF-β, play a role in excessive collagen production.•Recent studies have supported a role for Fibronectin Extra Domain A (Fn-EDA) which is markedly upregulated in keloids.•Identification of pathways involved in matrix accumulation allows development of targeted therapies for fibrotic diseases.</description><identifier>ISSN: 0945-053X</identifier><identifier>EISSN: 1569-1802</identifier><identifier>DOI: 10.1016/j.matbio.2016.01.013</identifier><identifier>PMID: 26844756</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Collagen ; Collagen - metabolism ; Extracellular Matrix - metabolism ; Extracellular Matrix - pathology ; Fibroblasts - pathology ; Fibrosis - drug therapy ; Fibrosis - pathology ; Fibrosis - surgery ; Fibrotic disease ; Humans ; Inflammation ; Keloid ; Keloid - drug therapy ; Keloid - pathology ; Keloid - surgery ; Skin - injuries ; Skin - pathology ; Steroids - therapeutic use ; TGF-β ; Wound healing ; Wound Healing - drug effects</subject><ispartof>Matrix biology, 2016-04, Vol.51, p.37-46</ispartof><rights>2016 International Society of Matrix Biology</rights><rights>Copyright © 2016 International Society of Matrix Biology. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c529t-e10452274d8dc42470bd2370b687347df2e88bf1c1b890291f33454ab56f2a3c3</citedby><cites>FETCH-LOGICAL-c529t-e10452274d8dc42470bd2370b687347df2e88bf1c1b890291f33454ab56f2a3c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.matbio.2016.01.013$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26844756$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Andrews, Jonathan P.</creatorcontrib><creatorcontrib>Marttala, Jaana</creatorcontrib><creatorcontrib>Macarak, Edward</creatorcontrib><creatorcontrib>Rosenbloom, Joel</creatorcontrib><creatorcontrib>Uitto, Jouni</creatorcontrib><title>Keloids: The paradigm of skin fibrosis — Pathomechanisms and treatment</title><title>Matrix biology</title><addtitle>Matrix Biol</addtitle><description>Keloids, fibroproliferative dermal tumors with effusive accumulation of extracellular matrix (ECM) components, particularly collagen, result from excessive expression of growth factors and cytokines. The etiology of keloids is unknown but they occur after dermal injury in genetically susceptible individuals, and they cause both physical and psychological distress for the affected individuals. Several treatment methods for keloids exist, including the combination therapy of surgical excision followed by intralesional steroid therapy, however, they have high recurrence rate regardless of the current treatment method. Improved understanding of the pathomechanisms leading to keloid formation will hopefully identify pathways that serve as specific targets to improve therapy for this devastating, currently intractable, disorder.
•Keloids are dermal tumors characterized by excessive accumulation of collagen.•The key cell responsible for matrix production is activated myofibroblast.•A number of growth factors, particularly TGF-β, play a role in excessive collagen production.•Recent studies have supported a role for Fibronectin Extra Domain A (Fn-EDA) which is markedly upregulated in keloids.•Identification of pathways involved in matrix accumulation allows development of targeted therapies for fibrotic diseases.</description><subject>Collagen</subject><subject>Collagen - metabolism</subject><subject>Extracellular Matrix - metabolism</subject><subject>Extracellular Matrix - pathology</subject><subject>Fibroblasts - pathology</subject><subject>Fibrosis - drug therapy</subject><subject>Fibrosis - pathology</subject><subject>Fibrosis - surgery</subject><subject>Fibrotic disease</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Keloid</subject><subject>Keloid - drug therapy</subject><subject>Keloid - pathology</subject><subject>Keloid - surgery</subject><subject>Skin - injuries</subject><subject>Skin - pathology</subject><subject>Steroids - therapeutic use</subject><subject>TGF-β</subject><subject>Wound healing</subject><subject>Wound Healing - drug effects</subject><issn>0945-053X</issn><issn>1569-1802</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UctuFDEQtCIQWQJ_ECEfuczG7ceMhwMSivISkeAQJG6Wx-7JepkZL_ZspNzyEfnCfAmONgS4ILXsbrm7ql1FyCGwJTCoj9bL0c5diEteqiWDEmKPLEDVbQWa8RdkwVqpKqbE933yOuc1Y0zKRr8i-7zWJVP1gpx_xiEGnz_QqxXSjU3Wh-uRxp7mH2GifehSzCHTh7t7-tXOqziiW9kp5DFTO3k6J7TziNP8hrzs7ZDx7dN9QL6dnlwdn1eXX84ujj9dVk7xdq4QmFScN9Jr7ySXDes8F-WsdSNk43uOWnc9OOh0y3gLvRBSSdupuudWOHFAPu5wN9tuRO8KdbKD2aQw2nRrog3m35cprMx1vDFSSw5KFoD3TwAp_txins0YssNhsBPGbTbQaNECB9ClVe5aXREhJ-yfaYCZRxPM2uxMMI8mGAYlRBl79_eKz0O_Vf_zByxC3QRMJruAk0MfErrZ-Bj-z_ALIp-bbA</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Andrews, Jonathan P.</creator><creator>Marttala, Jaana</creator><creator>Macarak, Edward</creator><creator>Rosenbloom, Joel</creator><creator>Uitto, Jouni</creator><general>Elsevier 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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160401</creationdate><title>Keloids: The paradigm of skin fibrosis — Pathomechanisms and treatment</title><author>Andrews, Jonathan P. ; Marttala, Jaana ; Macarak, Edward ; Rosenbloom, Joel ; Uitto, Jouni</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c529t-e10452274d8dc42470bd2370b687347df2e88bf1c1b890291f33454ab56f2a3c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Collagen</topic><topic>Collagen - metabolism</topic><topic>Extracellular Matrix - metabolism</topic><topic>Extracellular Matrix - pathology</topic><topic>Fibroblasts - pathology</topic><topic>Fibrosis - drug therapy</topic><topic>Fibrosis - pathology</topic><topic>Fibrosis - surgery</topic><topic>Fibrotic disease</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Keloid</topic><topic>Keloid - drug therapy</topic><topic>Keloid - pathology</topic><topic>Keloid - surgery</topic><topic>Skin - injuries</topic><topic>Skin - pathology</topic><topic>Steroids - therapeutic use</topic><topic>TGF-β</topic><topic>Wound healing</topic><topic>Wound Healing - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Andrews, Jonathan P.</creatorcontrib><creatorcontrib>Marttala, Jaana</creatorcontrib><creatorcontrib>Macarak, Edward</creatorcontrib><creatorcontrib>Rosenbloom, Joel</creatorcontrib><creatorcontrib>Uitto, Jouni</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Matrix biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Andrews, Jonathan P.</au><au>Marttala, Jaana</au><au>Macarak, Edward</au><au>Rosenbloom, Joel</au><au>Uitto, Jouni</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Keloids: The paradigm of skin fibrosis — Pathomechanisms and treatment</atitle><jtitle>Matrix biology</jtitle><addtitle>Matrix Biol</addtitle><date>2016-04-01</date><risdate>2016</risdate><volume>51</volume><spage>37</spage><epage>46</epage><pages>37-46</pages><issn>0945-053X</issn><eissn>1569-1802</eissn><abstract>Keloids, fibroproliferative dermal tumors with effusive accumulation of extracellular matrix (ECM) components, particularly collagen, result from excessive expression of growth factors and cytokines. The etiology of keloids is unknown but they occur after dermal injury in genetically susceptible individuals, and they cause both physical and psychological distress for the affected individuals. Several treatment methods for keloids exist, including the combination therapy of surgical excision followed by intralesional steroid therapy, however, they have high recurrence rate regardless of the current treatment method. Improved understanding of the pathomechanisms leading to keloid formation will hopefully identify pathways that serve as specific targets to improve therapy for this devastating, currently intractable, disorder.
•Keloids are dermal tumors characterized by excessive accumulation of collagen.•The key cell responsible for matrix production is activated myofibroblast.•A number of growth factors, particularly TGF-β, play a role in excessive collagen production.•Recent studies have supported a role for Fibronectin Extra Domain A (Fn-EDA) which is markedly upregulated in keloids.•Identification of pathways involved in matrix accumulation allows development of targeted therapies for fibrotic diseases.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>26844756</pmid><doi>10.1016/j.matbio.2016.01.013</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Collagen Collagen - metabolism Extracellular Matrix - metabolism Extracellular Matrix - pathology Fibroblasts - pathology Fibrosis - drug therapy Fibrosis - pathology Fibrosis - surgery Fibrotic disease Humans Inflammation Keloid Keloid - drug therapy Keloid - pathology Keloid - surgery Skin - injuries Skin - pathology Steroids - therapeutic use TGF-β Wound healing Wound Healing - drug effects |
title | Keloids: The paradigm of skin fibrosis — Pathomechanisms and treatment |
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