Key result
PAR-2 emerges as a novel respiratory therapeutic target by modulating airway inflammation and smooth muscle relaxation.
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This review highlights the critical, dual roles of proteinase-activated receptors (particularly PAR-2) in respiratory physiology and inflammation, identifying them as potential therapeutic targets for asthma and COPD.
Proteinase-activated receptors (PARs), a family of G protein-coupled receptors, are widely distributed in the mammalian body, playing a variety of physiological/pathophysiological roles. In the respiratory systems, PARs, particularly PAR-2 and PAR-1, are expressed in the epithelial and smooth muscle cells. In addition to the G(q/11)-mediated activation of the phospholipase C beta pathway, epithelial PAR activation causes prompt and/or delayed prostanoid formation, leading to airway smooth muscle relaxation and/or modulation of an inflammatory process. PAR-2 present in the epithelium and smooth muscle is considered primarily pro-inflammatory in the respiratory system, although PAR-2 may also be anti-inflammatory under certain conditions. In the lung epithelial cells, PAR-2 can also be activated by exogenous proteinases including house dust mite allergens, in addition to various possible endogenous agonist proteinases. Clinical evidence also suggests possible involvement of PARs, particularly PAR-2, in respiratory diseases. PARs thus appear to play critical roles in the respiratory systems, and the agonists/antagonists for PARs may serve as the novel therapeutic strategy for treatment of certain respiratory diseases including asthma.
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Kawabata et al. (2005) conducted a review in Respiratory diseases (e.g., asthma, COPD). Proteinase-Activated Receptors (PARs) modulators was evaluated. Proteinase-activated receptors, particularly PAR-2, play critical dual roles in airway inflammation and smooth muscle relaxation, suggesting they may serve as novel therapeutic targets for respiratory diseases.
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