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表皮生长因子受体在银屑病中作用的最新进展

Recent advances on the roles of epidermal growth factor receptor in psoriasis.

作者信息

Wang Sijia, Zhang Zhuoli, Peng Han, Zeng Kang

机构信息

Department of Dermatology, Nanfang Hospital, Southern Medical University Guangzhou 510515, Guangdong, China.

Department of Dermatology, Feinberg School of Medicine, Northwestern University Chicago 60611, IL, USA.

出版信息

Am J Transl Res. 2019 Feb 15;11(2):520-528. eCollection 2019.

Abstract

Epidermal growth factor receptor (EGFR) is a well-characterized receptor tyrosine kinase that involved in many vital activities in cell development, such as cellular homeostasis, proliferation, division, differentiation and apoptosis. Natural activation of EGFR and the concomitant downstream signaling pathways regulation are substantial to maintain normal cellular functions. In recent studies, EGFR was demonstrated to be a fundamental modulator in the control of skin inflammatory responses. Several dermatologic diseases including psoriasis are related to the anomalous activation of EGFR signaling. It has been proved that the expression and activity of EGFR and its endogenous ligands are overexpressed in the active epidermis lesions of psoriasis. Moreover, the remarkable therapeutic improvement of chronic psoriasis in cancer patients during the treatment of EGFR inhibitors or anti-EGFR monoclonal antibodies are also recorded, suggesting that the EGFR-mediated signaling may conduct a crucial role in the pathophysiology of psoriasis.

摘要

表皮生长因子受体(EGFR)是一种特征明确的受体酪氨酸激酶,参与细胞发育中的许多重要活动,如细胞内稳态、增殖、分裂、分化和凋亡。EGFR的自然激活以及随之而来的下游信号通路调节对于维持正常细胞功能至关重要。在最近的研究中,EGFR被证明是控制皮肤炎症反应的一个基本调节因子。包括银屑病在内的几种皮肤病与EGFR信号的异常激活有关。已经证明,EGFR及其内源性配体的表达和活性在银屑病的活动性表皮病变中过度表达。此外,在使用EGFR抑制剂或抗EGFR单克隆抗体治疗期间,癌症患者慢性银屑病的显著治疗改善也有记录,这表明EGFR介导的信号可能在银屑病的病理生理学中起关键作用。

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本文引用的文献

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A systematic review of worldwide epidemiology of psoriasis.银屑病全球流行病学的系统评价。
J Eur Acad Dermatol Venereol. 2017 Feb;31(2):205-212. doi: 10.1111/jdv.13854. Epub 2016 Aug 30.
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Psoriasis.银屑病。
Lancet. 2015 Sep 5;386(9997):983-94. doi: 10.1016/S0140-6736(14)61909-7. Epub 2015 May 27.

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