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1
TWEAK Progress in Dermatology: A Review.TWEAK在皮肤病学领域的进展:综述
Indian J Dermatol. 2023 Jul-Aug;68(4):425-429. doi: 10.4103/ijd.ijd_885_22.
2
Role of the TWEAK/Fn14 pathway in autoimmune diseases.TWEAK/Fn14信号通路在自身免疫性疾病中的作用。
Immunol Res. 2016 Feb;64(1):44-50. doi: 10.1007/s12026-015-8761-y.
3
TWEAK/Fn14 Activation Participates in Skin Inflammation.TWEAK/Fn14 激活参与皮肤炎症。
Mediators Inflamm. 2017;2017:6746870. doi: 10.1155/2017/6746870. Epub 2017 Sep 6.
4
Experimental atopic dermatitis is dependent on the TWEAK/Fn14 signaling pathway.实验性特应性皮炎依赖于 TWEAK/Fn14 信号通路。
Clin Exp Immunol. 2020 Jan;199(1):56-67. doi: 10.1111/cei.13373. Epub 2019 Sep 17.
5
TWEAK/Fn14 activation induces keratinocyte proliferation under psoriatic inflammation.TWEAK/Fn14激活在银屑病炎症状态下诱导角质形成细胞增殖。
Exp Dermatol. 2016 Jan;25(1):32-7. doi: 10.1111/exd.12820. Epub 2015 Sep 15.
6
The TNF-like weak inducer of the apoptosis/fibroblast growth factor-inducible molecule 14 axis mediates histamine and platelet-activating factor-induced subcutaneous vascular leakage and anaphylactic shock.肿瘤坏死因子样凋亡/成纤维细胞生长因子诱导分子 14 轴的弱诱导剂介导组胺和血小板激活因子诱导的皮下血管渗漏和过敏休克。
J Allergy Clin Immunol. 2020 Feb;145(2):583-596.e6. doi: 10.1016/j.jaci.2019.09.019. Epub 2019 Oct 31.
7
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8
Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling.肿瘤坏死因子受体介导成纤维细胞生长因子诱导蛋白14信号传导。
Cell Physiol Biochem. 2017;43(2):579-588. doi: 10.1159/000480530. Epub 2017 Sep 21.
9
Role of tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible 14 (Fn14) axis in rheumatic diseases.肿瘤坏死因子样凋亡弱诱导剂(TWEAK)/成纤维细胞生长因子诱导 14(Fn14)轴在风湿性疾病中的作用。
Chin Med J (Engl). 2012 Nov;125(21):3898-904.
10
Fn14 deficiency ameliorates psoriasis-like skin disease in a murine model.Fn14 缺乏可改善小鼠模型的银屑病样皮肤病。
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本文引用的文献

1
Involvement of the cytokine TWEAK in the pathogenesis of psoriasis vulgaris, pustular psoriasis, and erythrodermic psoriasis.细胞因子 TWEAK 在寻常型银屑病、脓疱型银屑病和红皮病型银屑病发病机制中的作用。
Cytokine. 2021 Feb;138:155391. doi: 10.1016/j.cyto.2020.155391. Epub 2020 Dec 8.
2
Serum TWEAK: A cutoff between segmental and nonsegmental vitiligo.血清肿瘤坏死因子样弱凋亡诱导因子:节段型与非节段型白癜风的分界点。
J Cosmet Dermatol. 2021 Mar;20(3):1017-1021. doi: 10.1111/jocd.13644. Epub 2020 Aug 17.
3
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in psoriasis and atopic dermatitis: A case-control study.银屑病和特应性皮炎中肿瘤坏死因子样凋亡弱诱导剂(TWEAK):一项病例对照研究。
J Am Acad Dermatol. 2021 Jun;84(6):1707-1708. doi: 10.1016/j.jaad.2020.08.004. Epub 2020 Aug 6.
4
Experimental atopic dermatitis is dependent on the TWEAK/Fn14 signaling pathway.实验性特应性皮炎依赖于 TWEAK/Fn14 信号通路。
Clin Exp Immunol. 2020 Jan;199(1):56-67. doi: 10.1111/cei.13373. Epub 2019 Sep 17.
5
Serum TWEAK in acne vulgaris: An unknown soldier.寻常痤疮患者血清 TWEAK 水平变化:一名无名战士。
J Cosmet Dermatol. 2020 Feb;19(2):514-518. doi: 10.1111/jocd.13011. Epub 2019 May 28.
6
The Growing Incidence of Bullous Pemphigoid: Overview and Potential Explanations.大疱性类天疱疮发病率的上升:概述与潜在解释
Front Med (Lausanne). 2018 Aug 20;5:220. doi: 10.3389/fmed.2018.00220. eCollection 2018.
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Systemic sclerosis.系统性硬化症。
Lancet. 2017 Oct 7;390(10103):1685-1699. doi: 10.1016/S0140-6736(17)30933-9. Epub 2017 Apr 13.
8
TWEAK/Fn14 Activation Contributes to the Pathogenesis of Bullous Pemphigoid.TWEAK/Fn14激活参与大疱性类天疱疮的发病机制。
J Invest Dermatol. 2017 Jul;137(7):1512-1522. doi: 10.1016/j.jid.2017.03.019. Epub 2017 Mar 27.
9
TWEAK activation of the non-canonical NF-κB signaling pathway differentially regulates melanoma and prostate cancer cell invasion.肿瘤坏死因子样弱凋亡诱导因子(TWEAK)激活非经典核因子κB(NF-κB)信号通路对黑色素瘤和前列腺癌细胞侵袭具有不同的调节作用。
Oncotarget. 2016 Dec 6;7(49):81474-81492. doi: 10.18632/oncotarget.13034.
10
Serum levels of TWEAK in patients with psoriasis vulgaris.寻常型银屑病患者的血清肿瘤坏死因子样弱凋亡诱导因子水平
Cytokine. 2016 Jan;77:10-3. doi: 10.1016/j.cyto.2015.10.004. Epub 2015 Oct 22.

TWEAK在皮肤病学领域的进展:综述

TWEAK Progress in Dermatology: A Review.

作者信息

Kharel Pramisha, Jia Chen, Dhital Kamal Raj, Chapagain Pukar, Aryal Sabita

机构信息

From the Department of Rheumatology and Immunology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China.

Department of Dermatology, Radiant Health Care, Kathmandu, Nepal.

出版信息

Indian J Dermatol. 2023 Jul-Aug;68(4):425-429. doi: 10.4103/ijd.ijd_885_22.

DOI:10.4103/ijd.ijd_885_22
PMID:37822396
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10564194/
Abstract

Tumour necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a member of the TNF superfamily (TNFSF). It acts through its receptor fibroblast growth factor-inducible 14 (Fn14). Studies have indicated that TWEAK/Fn14 pathway activation controls multiple cellular responses, including proliferation, angiogenesis and induction of inflammatory cytokines. TWEAK/Fn14 is manifested in many tissues of our body and most importantly in the skin causing inflammation and many autoimmune and neoplastic cutaneous disorders. Evidence suggests that the TWEAK/Fn14 axis, the downstream signalling pathway and its inflammatory molecular expressions are involved in the pathogenesis of many cutaneous disorders such as psoriasis, atopic dermatitis (AD) vitiligo and melanoma. So, this literature review describes a brief introduction of TWEAK and TWEAK/Fn14 pathway and summarises the case-series and open-label studies performed in the field of dermatology and its potential therapeutic benefit.

摘要

肿瘤坏死因子(TNF)样凋亡微弱诱导剂(TWEAK)是肿瘤坏死因子超家族(TNFSF)的成员。它通过其受体成纤维细胞生长因子诱导14(Fn14)发挥作用。研究表明,TWEAK/Fn14通路激活可控制多种细胞反应,包括增殖、血管生成和炎症细胞因子的诱导。TWEAK/Fn14在我们身体的许多组织中都有表现,最重要的是在皮肤中,会导致炎症以及许多自身免疫性和肿瘤性皮肤疾病。有证据表明,TWEAK/Fn14轴、下游信号通路及其炎症分子表达参与了许多皮肤疾病的发病机制,如银屑病、特应性皮炎(AD)、白癜风和黑色素瘤。因此,这篇文献综述简要介绍了TWEAK和TWEAK/Fn14通路,并总结了在皮肤病学领域进行的病例系列研究和开放标签研究及其潜在的治疗益处。