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NADPH oxidases—do they play a role in TRPC regulation under hypoxia?
- 作者：Monika Malczyk ; Christine Veith…
- 关键词：NADPH oxidases ; Reactive oxygen species ; Transient receptor potential channels ; Hypoxic pulmonary vasoconstriction ; Pulmonary hypertension ; Pulmonary vascular remodelling
- 刊名：Pfl¨¹gers Archiv - European Journal of Physiology
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：468
- 期：1
- 页码：23-41
- 全文大小：1,639 KB
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- 作者单位：Monika Malczyk (1)
Christine Veith (1)
Ralph T. Schermuly (1)
Thomas Gudermann (2)
Alexander Dietrich (2)
Natascha Sommer (1)
Norbert Weissmann (1)
Oleg Pak (1)
1. Universities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardiopulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Aulweg 130, 35392, Giessen, Germany
2. Walther-Straub-Institute for Pharmacology and Toxicology, Ludwig-Maximilians University Munich, Member of the German Center for Lung Research (DZL), Munich, Germany
- 刊物主题：Human Physiology;
- 出版者：Springer Berlin Heidelberg
- ISSN：1432-2013
文摘
In the lung, acute alveolar hypoxia causes hypoxic pulmonary vasoconstriction (HPV) to maintain ventilation perfusion matching and thus optimal oxygenation of blood. In contrast, global chronic hypoxia triggers a pathological thickening of pulmonary arterial walls, called pulmonary vascular remodelling, leading to persistence of pulmonary hypertension (PH). Moreover, ischaemia or hypoxia can lead to a damage of pulmonary endothelial cells with subsequent oedema formation. Alterations in reactive oxygen species (ROS) have been suggested as a crucial mediator of such responses. Among the various sources of cellular ROS production, NADPH oxidases (NOXs) have been found to contribute to these physiological and pathophysiological signalling processes. NOXs are the only known examples that generate ROS as the primary function of the enzyme system. However, the downstream targets of NOX-derived ROS signalling in hypoxia are still not known. Canonical transient receptor potential (TRPC) channels recently have been recognised as directly or indirectly ROS-activated channels and have been shown to be essential for hypoxia-dependent vascular regulatory processes in the lung. Against this background, we here summarise the current knowledge on NOX-mediated TRPC channel signalling during hypoxia in the pulmonary circulation. Keywords NADPH oxidases Reactive oxygen species Transient receptor potential channels Hypoxic pulmonary vasoconstriction Pulmonary hypertension Pulmonary vascular remodelling
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