STAT3 targeting in dystrophic epidermolysis bullosa
STAT3 targeting in dystrophic epidermolysis bullosa
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STAT3靶向治疗营养不良性大疱性表皮松解症
DOI：
10.1111/bjd.18639
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发表时间：
2020
影响因子：
10.3
通讯作者：
Gaggioli C
中科院分区：
文献类型：
--
作者：
Mittapalli VR;Kühl T;Kuzet SE;Gretzmeier C;Kiritsi D;Gaggioli C
亲爱的编辑，营养不良性大疱性表皮病（DEB）是一种皮肤起泡性疾病，由编码锚定纤维成分胶原VII的COL 7A 1基因突变引起。1继发于皮肤脆性，DEB表现为慢性伤口和进行性软组织纤维化。由于皮肤微环境的长期损伤和硬化，患有严重DEB的人容易发展为早发性转移性皮肤鳞状细胞癌（cSCC）。1，2 DEB中的皮肤纤维化是损伤和炎症驱动的纤维化过程激活的典型（Nyström和Bruckner-Tuderman，以及其中的参考文献）。2转化生长因子（Transforming growth factor，TGF）-B和白细胞介素（interleukin，IL）-6被认为介导了DEB中的纤维化。1，3 Janus激酶（JAK）1/2-信号转导子和转录激活子3（STAT 3）信号通路是（a）（c）（d）（B）的重要下游导体。
DEAR EDITOR, Dystrophic epidermolysis bullosa (DEB) is a skinblistering disease caused by mutations in the COL7A1 gene encoding the anchoring fibril-constituent collagen VII. 1 Secondary to skin fragility, DEB manifests as chronic wounds and progressive soft tissue fibrosis. As a consequence of a chronically injured and stiffened dermal microenvironment people with severe DEB are prone to developing early-onset metastatic cutaneous squamous cell carcinomas (cSCCs). 1, 2 Dermal fibrosis in DEB is paradigmatic of injury-and inflammation-driven activation of fibrogenic processes (Nyström and Bruckner-Tuderman, and references therein). 2 Transforming growth factor (TGF)-b and interleukin (IL)-6 have been suggested to mediate fibrosis in DEB. 1, 3 The Janus kinase (JAK) 1/2–signal transducers and activators of transcription 3 (STAT3) signalling pathway is a prominent downstream conductor of (a)(c)(d)(b)
影响因子：
16.6
作者：
Zehender A;Huang J;Györfi AH;Matei AE;Trinh-Minh T;Xu X;Li YN;Chen CW;Lin J;Dees C;Beyer C;Gelse K;Zhang ZY;Bergmann C;Ramming A;Birchmeier W;Distler O;Schett G;Distler JHW
通讯作者：
Distler JHW
影响因子：
11.2
作者：
Mittapalli, Venugopal R.;Madl, Josef;Bruckner-Tuderman, Leena
通讯作者：
Bruckner-Tuderman, Leena