Cargando…

Cell Adhesion Molecules in Fibrotic Diseases

Mechanisms underlying the pathogenesis of tissue fibrosis remain incompletely understood. Emerging evidence suggests that cell adhesion molecules (CAMs) are critical in fibrotic progression in many organs, including lung, kidney, skin, and liver. CAMs promote cell–cell and cell–extracellular matrix...

Descripción completa

Detalles Bibliográficos
Autores principales: Hu, Qianjiang, Saleem, Komal, Pandey, Jyotsana, Charania, Arzoo N., Zhou, Yong, He, Chao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10377070/
https://www.ncbi.nlm.nih.gov/pubmed/37509634
http://dx.doi.org/10.3390/biomedicines11071995
_version_ 1785079425592721408
author Hu, Qianjiang
Saleem, Komal
Pandey, Jyotsana
Charania, Arzoo N.
Zhou, Yong
He, Chao
author_facet Hu, Qianjiang
Saleem, Komal
Pandey, Jyotsana
Charania, Arzoo N.
Zhou, Yong
He, Chao
author_sort Hu, Qianjiang
collection PubMed
description Mechanisms underlying the pathogenesis of tissue fibrosis remain incompletely understood. Emerging evidence suggests that cell adhesion molecules (CAMs) are critical in fibrotic progression in many organs, including lung, kidney, skin, and liver. CAMs promote cell–cell and cell–extracellular matrix (ECM) interactions to maintain tissue architecture and normal function in homeostasis. However, dysregulated expression and function of CAMs can lead to chronic inflammation and tissue fibrosis. The major families of CAMs include integrins, cadherins, selectins, and immunoglobulins. Here, we review the role of the CAMs in fibrosis development across various organs with a focus on integrins and cadherins, and discuss their respective roles in the development of pulmonary fibrosis.
format Online
Article
Text
id pubmed-10377070
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-103770702023-07-29 Cell Adhesion Molecules in Fibrotic Diseases Hu, Qianjiang Saleem, Komal Pandey, Jyotsana Charania, Arzoo N. Zhou, Yong He, Chao Biomedicines Review Mechanisms underlying the pathogenesis of tissue fibrosis remain incompletely understood. Emerging evidence suggests that cell adhesion molecules (CAMs) are critical in fibrotic progression in many organs, including lung, kidney, skin, and liver. CAMs promote cell–cell and cell–extracellular matrix (ECM) interactions to maintain tissue architecture and normal function in homeostasis. However, dysregulated expression and function of CAMs can lead to chronic inflammation and tissue fibrosis. The major families of CAMs include integrins, cadherins, selectins, and immunoglobulins. Here, we review the role of the CAMs in fibrosis development across various organs with a focus on integrins and cadherins, and discuss their respective roles in the development of pulmonary fibrosis. MDPI 2023-07-14 /pmc/articles/PMC10377070/ /pubmed/37509634 http://dx.doi.org/10.3390/biomedicines11071995 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Hu, Qianjiang
Saleem, Komal
Pandey, Jyotsana
Charania, Arzoo N.
Zhou, Yong
He, Chao
Cell Adhesion Molecules in Fibrotic Diseases
title Cell Adhesion Molecules in Fibrotic Diseases
title_full Cell Adhesion Molecules in Fibrotic Diseases
title_fullStr Cell Adhesion Molecules in Fibrotic Diseases
title_full_unstemmed Cell Adhesion Molecules in Fibrotic Diseases
title_short Cell Adhesion Molecules in Fibrotic Diseases
title_sort cell adhesion molecules in fibrotic diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10377070/
https://www.ncbi.nlm.nih.gov/pubmed/37509634
http://dx.doi.org/10.3390/biomedicines11071995
work_keys_str_mv AT huqianjiang celladhesionmoleculesinfibroticdiseases
AT saleemkomal celladhesionmoleculesinfibroticdiseases
AT pandeyjyotsana celladhesionmoleculesinfibroticdiseases
AT charaniaarzoon celladhesionmoleculesinfibroticdiseases
AT zhouyong celladhesionmoleculesinfibroticdiseases
AT hechao celladhesionmoleculesinfibroticdiseases