作者: Reinoud Gosens , Johan Zaagsma , Mechteld Grootte Bromhaar , Adriaan Nelemans , Herman Meurs
DOI: 10.1016/J.EJPHAR.2004.07.025
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摘要: Abstract Increased airway smooth muscle mass is a pathological feature that asthma and chronic obstructive pulmonary disease (COPD) have in common. This increase has gained renewed interest view of recent developments showing muscle, instead solely being contractile partner, capable interacting dynamically with its environment, especially under inflammatory conditions. Airway cells are able to proliferate, migrate, secrete chemokines, cytokines, extracellular matrix proteins growth factors, most importantly, adapt these functions by changing phenotype from proliferative/synthetic. Conversely, switching (hyper)contractile may also occur. A vast number stimuli regulate exert their effects via excitatory Gq or Gi-coupled receptors. Since acetylcholine activates muscarinic M2 M3 receptors the cell membrane, which coupled Gi proteins, respectively, since release be enhanced inflammation, pathophysiological role related above processes exceeding contraction could envisaged. In this review, evidence favour hypothesis, based on data show for modulating proliferation, contractility protein expression discussed. Based findings, we postulate endogenous contributes remodeling COPD.