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There is a strong genetic predisposition for keloid formation, and individuals of African and Asian ancestry are particularly prone. The principal cell type responsible for ECM accumulation is the myofibroblast derived from quiescent resident skin fibroblasts either through\n                    <jats:italic>trans<\/jats:italic>\n                    \u2010differentiation or from keloid progenitor stem cells with capacity for multi\u2010lineage differentiation and self\u2010renewal. The biosynthetic pathways leading to ECM accumulation are activated by several cytokines, but particularly by TGF\u2010\u03b2 signalling. The mechanical properties of the cellular microenvironment also play a critical role in the cell's response to TGF\u2010\u03b2, as demonstrated by culturing of fibroblasts derived from keloids and control skin on substrata with different degrees of stiffness. These studies also demonstrated that culturing of fibroblasts on tissue culture plastic in vitro does not reflect their biosynthetic capacity in vivo. Collectively, our current understanding of the pathogenesis of keloids suggests a complex network of interacting cellular, molecular and mechanical factors, with distinct pathways leading to myofibroblast differentiation and activation. Keloids can serve as a model system of fibrotic diseases, a group of currently intractable disorders, and deciphering of the critical pathogenetic steps leading to ECM accumulation is expected to identify targets for pharmacologic intervention, not only for keloids but also for a number of other, both genetic and acquired, fibrotic diseases.\n                  <\/jats:p>","DOI":"10.1111\/exd.14243","type":"journal-article","created":{"date-parts":[[2020,11,20]],"date-time":"2020-11-20T01:01:09Z","timestamp":1605834069000},"page":"132-145","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":137,"title":["Keloid disorder: Fibroblast differentiation and gene expression profile in fibrotic skin diseases"],"prefix":"10.1111","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2557-7538","authenticated-orcid":false,"given":"Edward J.","family":"Macarak","sequence":"first","affiliation":[{"name":"The Joan and Joel Rosenbloom Center for Fibrotic Diseases and the Jefferson Institute of Molecular Medicine Department of Dermatology and Cutaneous Biology Sidney Kimmel Medical College at Thomas Jefferson University Philadelphia PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0242-7265","authenticated-orcid":false,"given":"Peter J.","family":"Wermuth","sequence":"additional","affiliation":[{"name":"The Joan and Joel Rosenbloom Center for Fibrotic Diseases and the Jefferson Institute of Molecular Medicine Department of Dermatology and Cutaneous Biology Sidney Kimmel Medical College at Thomas Jefferson University Philadelphia PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joel","family":"Rosenbloom","sequence":"additional","affiliation":[{"name":"The Joan and Joel Rosenbloom Center for Fibrotic Diseases and the Jefferson Institute of Molecular Medicine Department of Dermatology and Cutaneous Biology Sidney Kimmel Medical College at Thomas Jefferson University Philadelphia PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4639-807X","authenticated-orcid":false,"given":"Jouni","family":"Uitto","sequence":"additional","affiliation":[{"name":"The Joan and Joel Rosenbloom Center for Fibrotic Diseases and the Jefferson Institute of Molecular Medicine Department of Dermatology and Cutaneous Biology Sidney Kimmel Medical College at Thomas Jefferson University Philadelphia PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2020,12,20]]},"reference":[{"key":"e_1_2_15_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jid.2019.10.002"},{"key":"e_1_2_15_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/wrr.12397"},{"key":"e_1_2_15_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.matbio.2016.01.014"},{"issue":"2","key":"e_1_2_15_5_1","first-page":"544","article-title":"NEDD4 single nucleotide polymorphism rs2271289 is associated with keloids in Chinese Han population","volume":"8","author":"Zhao Y","year":"2016","journal-title":"Am J Transl Res"},{"key":"e_1_2_15_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jid.2018.09.007"},{"key":"e_1_2_15_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jid.2018.07.044"},{"key":"e_1_2_15_8_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.0022-202X.2004.22327.x"},{"key":"e_1_2_15_9_1","doi-asserted-by":"publisher","DOI":"10.1001\/archderm.137.11.1429"},{"key":"e_1_2_15_10_1","doi-asserted-by":"publisher","DOI":"10.1111\/iep.12198"},{"key":"e_1_2_15_11_1","doi-asserted-by":"publisher","DOI":"10.1007\/s11033-019-05120-y"},{"key":"e_1_2_15_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2019.111799"},{"issue":"1","key":"e_1_2_15_13_1","first-page":"105","article-title":"Morphological and immunochemical differences between keloid and hypertrophic scar","volume":"145","author":"Ehrlich HP","year":"1994","journal-title":"Am J Pathol"},{"issue":"1","key":"e_1_2_15_14_1","first-page":"65","article-title":"Histologic basis of keloid and hypertrophic scar differentiation. 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