Abstract
1. Severe persistent asthma is accompanied by structural changes in the airway, referred to as remodelling. The mechanisms driving airway remodelling are poorly understood. 2. Transforming growth factor (TGF)-beta is increased in the airways of patients with asthma. Many of the effects of TGF-beta are mediated by connective tissue growth factor (CTGF). 3. Overexpression of CTGF is linked to many fibrotic diseases, but its exact role in airway remodelling is unknown. 4. Connective tissue growth factor mediates cell adhesion, migration, proliferation, survival, extracellular matrix synthesis and has a role in angiogenesis. 5. Current asthma therapies do not inhibit CTGF induction. 6. Understanding the mechanisms underlying the role of CTGF in airway remodelling may lead to new therapeutic strategies for asthma.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Anti-Asthmatic Agents / pharmacology
-
Anti-Asthmatic Agents / therapeutic use
-
Asthma / drug therapy
-
Asthma / metabolism*
-
Asthma / pathology
-
Connective Tissue Growth Factor
-
Extracellular Matrix / drug effects
-
Extracellular Matrix / metabolism
-
Extracellular Matrix Proteins / metabolism
-
Gene Expression / drug effects
-
Humans
-
Immediate-Early Proteins / genetics
-
Immediate-Early Proteins / metabolism*
-
Integrins / metabolism
-
Intercellular Signaling Peptides and Proteins / genetics
-
Intercellular Signaling Peptides and Proteins / metabolism*
-
Myocytes, Smooth Muscle / drug effects
-
Myocytes, Smooth Muscle / metabolism
-
Receptors, Cell Surface / metabolism
-
Signal Transduction / drug effects
-
Transforming Growth Factor beta / metabolism
-
Transforming Growth Factor beta / pharmacology
Substances
-
Anti-Asthmatic Agents
-
CCN2 protein, human
-
Extracellular Matrix Proteins
-
Immediate-Early Proteins
-
Integrins
-
Intercellular Signaling Peptides and Proteins
-
Receptors, Cell Surface
-
Transforming Growth Factor beta
-
Connective Tissue Growth Factor