Progress of ADAM17 in Fibrosis-Related Diseases

Fibrosis leads to structural damage and functional decline and is characterized by an accumulation of fibrous connective tissue and a reduction in parenchymal cells. Because of its extremely poor prognosis, organ fibrosis poses a significant economic burden. In order to prevent and treat fibrosis mo...

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Main Authors: Suyan Yan, Yaqi Zhao, Yuyu Yang, Baocheng Liu, Wei Xu, Zhenzhen Ma, Qingrui Yang
Format: Article
Language:English
Published: Wiley 2025-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/mi/9999723
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author Suyan Yan
Yaqi Zhao
Yuyu Yang
Baocheng Liu
Wei Xu
Zhenzhen Ma
Qingrui Yang
author_facet Suyan Yan
Yaqi Zhao
Yuyu Yang
Baocheng Liu
Wei Xu
Zhenzhen Ma
Qingrui Yang
author_sort Suyan Yan
collection DOAJ
description Fibrosis leads to structural damage and functional decline and is characterized by an accumulation of fibrous connective tissue and a reduction in parenchymal cells. Because of its extremely poor prognosis, organ fibrosis poses a significant economic burden. In order to prevent and treat fibrosis more effectively, potential mechanisms need to be investigated. A disintegrin and metalloprotease 17 (ADAM17) is a membrane-bound protein. It regulates intracellular signaling and membrane protein degradation. Fibrosis mediated by ADAM17 has been identified as an important contributor, although the specific relationship between its multiple regulatory functions and the pathogenesis is unclear. This article describes ADAM17 activation, function, and regulation, as well as the role of ADAM17 mediated fibrosis injury in kidney, liver, heart, lung, skin, endometrium, and retina. To develop new therapeutic approaches based on ADAM17 related signal pathways.
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id doaj-art-18945e85ed544a8a9f6a2e12e5cf1a58
institution OA Journals
issn 1466-1861
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publishDate 2025-01-01
publisher Wiley
record_format Article
series Mediators of Inflammation
spelling doaj-art-18945e85ed544a8a9f6a2e12e5cf1a582025-08-20T02:09:32ZengWileyMediators of Inflammation1466-18612025-01-01202510.1155/mi/9999723Progress of ADAM17 in Fibrosis-Related DiseasesSuyan Yan0Yaqi Zhao1Yuyu Yang2Baocheng Liu3Wei Xu4Zhenzhen Ma5Qingrui Yang6Department of Rheumatology and ImmunologyDepartment of Rheumatology and ImmunologyUCL School of PharmacyDepartment of Rheumatology and ImmunologyDepartment of Rheumatology and ImmunologyDepartment of Rheumatology and ImmunologyDepartment of Rheumatology and ImmunologyFibrosis leads to structural damage and functional decline and is characterized by an accumulation of fibrous connective tissue and a reduction in parenchymal cells. Because of its extremely poor prognosis, organ fibrosis poses a significant economic burden. In order to prevent and treat fibrosis more effectively, potential mechanisms need to be investigated. A disintegrin and metalloprotease 17 (ADAM17) is a membrane-bound protein. It regulates intracellular signaling and membrane protein degradation. Fibrosis mediated by ADAM17 has been identified as an important contributor, although the specific relationship between its multiple regulatory functions and the pathogenesis is unclear. This article describes ADAM17 activation, function, and regulation, as well as the role of ADAM17 mediated fibrosis injury in kidney, liver, heart, lung, skin, endometrium, and retina. To develop new therapeutic approaches based on ADAM17 related signal pathways.http://dx.doi.org/10.1155/mi/9999723
spellingShingle Suyan Yan
Yaqi Zhao
Yuyu Yang
Baocheng Liu
Wei Xu
Zhenzhen Ma
Qingrui Yang
Progress of ADAM17 in Fibrosis-Related Diseases
Mediators of Inflammation
title Progress of ADAM17 in Fibrosis-Related Diseases
title_full Progress of ADAM17 in Fibrosis-Related Diseases
title_fullStr Progress of ADAM17 in Fibrosis-Related Diseases
title_full_unstemmed Progress of ADAM17 in Fibrosis-Related Diseases
title_short Progress of ADAM17 in Fibrosis-Related Diseases
title_sort progress of adam17 in fibrosis related diseases
url http://dx.doi.org/10.1155/mi/9999723
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AT weixu progressofadam17infibrosisrelateddiseases
AT zhenzhenma progressofadam17infibrosisrelateddiseases
AT qingruiyang progressofadam17infibrosisrelateddiseases