PARs in the Respiratory System: Cellular Signaling and Physiological/Pathological Roles
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- Kawabata Atsufumi
- Division of Physiology & Pathophysiology, School of Pharmaceutical Sciences, Kinki University
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- Kawao Naoyuki
- Division of Physiology & Pathophysiology, School of Pharmaceutical Sciences, Kinki University
書誌事項
- タイトル別名
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- Physiology and Pathophysiology of Proteinase-Activated Receptors (PARs): PARs in the Respiratory System: Cellular Signaling and Physiological/Pathological Roles
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抄録
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 Gq/11-mediated activation of the phospholipase C β 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.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 97 (1), 20-24, 2005
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205176176768
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- NII論文ID
- 10025724999
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 7228396
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- PubMed
- 15655298
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可