Abstract
Allergic asthma is a chronic airway inflammatory disorder attributable to T-helper 2 cell responses together with other inflammatory cells such as mast cells, B cells and eosinophils, and pro-inflammatory cytokines and chemokines. Mitogen-activated protein kinase (MAPK) signaling cascades have been shown to be important in the differentiation, activation, proliferation, degranulation and migration of various immune cells, and airway smooth muscle and epithelial cells. In mammal, MAPK signaling modules are divided into at least 3 groups: extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun NH2-terminal kinase (JNK). Each MAPK module plays a discrete yet complementary role in accentuating allergic airway inflammation. Cumulative evidence reveals potential anti-inflammatory activities of MAPK inhibitors in a variety of in vitro models of inflammation. Recently, the anti-inflammatory effects of MAPK kinase inhibitor (U0126), p38 MAPK inhibitors (SB239063 and respirable p38α MAPK antisense oligonucleotide) and JNK inhibitor (SP600125) have been demonstrated in in vivo animal models of asthma. Development of inhibitors targeting at MAPK could be an attractive strategy for the treatment of asthma.
Keywords: extracellular signal-regulated protein kinase, p38 MAPK, c-Jun NH2-terminal kinase, cytokine, immune receptor, chemokine, animal models, airway smooth muscle cells, epithelial cells
Current Drug Targets
Title: Targeting Mitogen-Activated Protein Kinases for Asthma
Volume: 7 Issue: 6
Author(s): Wei Duan and W.S. F. Wong
Affiliation:
Keywords: extracellular signal-regulated protein kinase, p38 MAPK, c-Jun NH2-terminal kinase, cytokine, immune receptor, chemokine, animal models, airway smooth muscle cells, epithelial cells
Abstract: Allergic asthma is a chronic airway inflammatory disorder attributable to T-helper 2 cell responses together with other inflammatory cells such as mast cells, B cells and eosinophils, and pro-inflammatory cytokines and chemokines. Mitogen-activated protein kinase (MAPK) signaling cascades have been shown to be important in the differentiation, activation, proliferation, degranulation and migration of various immune cells, and airway smooth muscle and epithelial cells. In mammal, MAPK signaling modules are divided into at least 3 groups: extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun NH2-terminal kinase (JNK). Each MAPK module plays a discrete yet complementary role in accentuating allergic airway inflammation. Cumulative evidence reveals potential anti-inflammatory activities of MAPK inhibitors in a variety of in vitro models of inflammation. Recently, the anti-inflammatory effects of MAPK kinase inhibitor (U0126), p38 MAPK inhibitors (SB239063 and respirable p38α MAPK antisense oligonucleotide) and JNK inhibitor (SP600125) have been demonstrated in in vivo animal models of asthma. Development of inhibitors targeting at MAPK could be an attractive strategy for the treatment of asthma.
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Cite this article as:
Duan Wei and Wong F. W.S., Targeting Mitogen-Activated Protein Kinases for Asthma, Current Drug Targets 2006; 7 (6) . https://dx.doi.org/10.2174/138945006777435353
DOI https://dx.doi.org/10.2174/138945006777435353 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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