RhoA, a Possible Target for Treatment of Airway Hyperresponsiveness in Bronchial Asthma
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- Chiba Yoshihiko
- Department of Pharmacology, School of Pharmacy, Hoshi University, Japan
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- Matsusue Kimihiko
- Faculty of Pharmaceutical Science, Fukuoka University, Japan
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- Misawa Miwa
- Department of Pharmacology, School of Pharmacy, Hoshi University, Japan
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Airway hyperresponsiveness to nonspecific stimuli is one of the characteristic features of allergic bronchial asthma. An elevated contractility of bronchial smooth muscle has been considered as one of the causes of the airway hyperresponsiveness. The contraction of smooth muscles including airway smooth muscles is mediated by both Ca2+-dependent and Ca2+-independent pathways. The latter Ca2+-independent pathway, termed Ca2+ sensitization, is mainly regulated by a monomeric GTP-binding protein, RhoA, and its downstream target Rho-kinase. In animal models of allergic bronchial asthma, an augmented agonist-induced, RhoA-mediated contraction of bronchial smooth muscle has been suggested. The RhoA/Rho-kinase signaling is now proposed as a novel target for the treatment of airway hyperresponsiveness in asthma. Herein, we will discuss the mechanism of development of bronchial smooth muscle hyperresponsiveness, one of the causes of the airway hyperresponsiveness, based on the recent studies using animal models of allergic bronchial asthma and/or cultured airway smooth muscle cells. The possibility of RhoA as a therapeutic target in asthma, especially airway hyperresponsiveness, will also be described.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 114 (3), 239-247, 2010
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
- 1390282680157332224
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- NII論文ID
- 10029890076
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 10887799
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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
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- 使用不可