Targeting cell signaling in allergic asthma

Asthma is chronic inflammation of the airways characterized by airway hyper-responsiveness, wheezing, cough, and dyspnea. Asthma affects >350 million people worldwide. The Th2 immune response is a major contributor to the pathophysiology of asthma. Targeted therapy modulating cell signaling pathw...

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Autor principal: Athari, Seyyed Shamsadin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Review Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6799822/
https://www.ncbi.nlm.nih.gov/pubmed/31637021
http://dx.doi.org/10.1038/s41392-019-0079-0
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author Athari, Seyyed Shamsadin
author_facet Athari, Seyyed Shamsadin
author_sort Athari, Seyyed Shamsadin
collection PubMed
description Asthma is chronic inflammation of the airways characterized by airway hyper-responsiveness, wheezing, cough, and dyspnea. Asthma affects >350 million people worldwide. The Th2 immune response is a major contributor to the pathophysiology of asthma. Targeted therapy modulating cell signaling pathways can be a powerful strategy to design new drugs to treat asthma. The potential molecular pathways that can be targeted include IL-4-IL-13-JAK-STAT-MAP kinases, adiponectin-iNOS-NF-κB, PGD2-CRTH2, IFNs-RIG, Wnt/β-catenin-FAM13A, FOXC1-miR-PI3K/AKT, JNK-Gal-7, Nrf2-ROS, Foxp3-RORγt, CysLTR, AMP, Fas-FasL, PTHrP/PPARγ, PAI-1, FcɛRI-LAT-SLP-76, Tim-3-Gal-9, TLRs-MyD88, PAR2, and Keap1/Nrf2/ARE. Therapeutic drugs can be designed to target one or more of these pathways to treat asthma.
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spelling pubmed-67998222019-10-21 Targeting cell signaling in allergic asthma Athari, Seyyed Shamsadin Signal Transduct Target Ther Review Article Asthma is chronic inflammation of the airways characterized by airway hyper-responsiveness, wheezing, cough, and dyspnea. Asthma affects >350 million people worldwide. The Th2 immune response is a major contributor to the pathophysiology of asthma. Targeted therapy modulating cell signaling pathways can be a powerful strategy to design new drugs to treat asthma. The potential molecular pathways that can be targeted include IL-4-IL-13-JAK-STAT-MAP kinases, adiponectin-iNOS-NF-κB, PGD2-CRTH2, IFNs-RIG, Wnt/β-catenin-FAM13A, FOXC1-miR-PI3K/AKT, JNK-Gal-7, Nrf2-ROS, Foxp3-RORγt, CysLTR, AMP, Fas-FasL, PTHrP/PPARγ, PAI-1, FcɛRI-LAT-SLP-76, Tim-3-Gal-9, TLRs-MyD88, PAR2, and Keap1/Nrf2/ARE. Therapeutic drugs can be designed to target one or more of these pathways to treat asthma. Nature Publishing Group UK 2019-10-18 /pmc/articles/PMC6799822/ /pubmed/31637021 http://dx.doi.org/10.1038/s41392-019-0079-0 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Review Article
Athari, Seyyed Shamsadin
Targeting cell signaling in allergic asthma
title Targeting cell signaling in allergic asthma
title_full Targeting cell signaling in allergic asthma
title_fullStr Targeting cell signaling in allergic asthma
title_full_unstemmed Targeting cell signaling in allergic asthma
title_short Targeting cell signaling in allergic asthma
title_sort targeting cell signaling in allergic asthma
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6799822/
https://www.ncbi.nlm.nih.gov/pubmed/31637021
http://dx.doi.org/10.1038/s41392-019-0079-0
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