Pharmacology of airway smooth muscle proliferation.
Airway smooth muscle thickening is a pathological feature that contributes significantly to airflow limitation and airway hyperresponsiveness in asthma. Ongoing research efforts aimed at identifying the mechanisms responsible for the increased airway smooth muscle mass have indicated that hyperplasia of airway smooth muscle, due in part to airway myocyte proliferation, is likely a major factor. Airway smooth muscle proliferation has been studied extensively in culture and in animal models of asthma, and these studies have revealed that a variety of receptors and mediators contributes to this response. This review aims to provide an overview of the receptors and mediators that control airway smooth muscle cell proliferation, with emphasis on the intracellular signalling mechanisms involved.
Gosens
Reinoud
R
Department of Molecular Pharmacology, University of Groningen, Groningen, The Netherlands. r.gosens@rug.nl
Roscioni
Sara S
SS
Dekkers
Bart G J
BG
Pera
Tonio
T
Schmidt
Martina
M
Schaafsma
Dedmer
D
Zaagsma
Johan
J
Meurs
Herman
H
D000818:Animals; D049109:Cell Proliferation / Q000187:drug effects; D016207:Cytokines / Q000502:physiology; D005109:Extracellular Matrix / Q000502:physiology; D006801:Humans; D016023:Integrins / Q000502:physiology; D020782:Matrix Metalloproteinases / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects*; D032389:Myocytes, Smooth Muscle / Q000187:drug effects*; D018377:Neurotransmitter Agents / Q000502:physiology; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000819:agonists; D012143:Respiratory Physiological Phenomena
D016207:Cytokines; D016023:Integrins; D018377:Neurotransmitter Agents; D043562:Receptors, G-Protein-Coupled; D011505:Protein-Tyrosine Kinases; D020782:Matrix Metalloproteinases