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dc.contributor.author | Gassmann, M. | |
dc.contributor.author | Cowburn, A. | |
dc.contributor.author | Gu, H. | |
dc.contributor.author | Li, J. | |
dc.contributor.author | Rodriguez, Marisela | |
dc.contributor.author | Babicheva, A. | |
dc.contributor.author | Jain, P.P. | |
dc.contributor.author | Xiong, M. | |
dc.contributor.author | Gassmann, N.N. | |
dc.contributor.author | Yuan, J.X.J. | |
dc.contributor.author | Wilkins, M.R. | |
dc.contributor.author | Zhao, L. | |
dc.date.accessioned | 2021-04-13T20:51:01Z | |
dc.date.available | 2021-04-13T20:51:01Z | |
dc.date.issued | 2020 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12866/9183 | |
dc.description.abstract | An increase in pulmonary artery pressure is a common observation in adult mammals exposed to global alveolar hypoxia. It is considered a maladaptive response that places an increased workload on the right ventricle. The mechanisms initiating and maintaining the elevated pressure are of considerable interest in understanding pulmonary vascular homeostasis. There is an expectation that identifying the key molecules in the integrated vascular response to hypoxia will inform potential drug targets. One strategy is to take advantage of experiments of nature, specifically, to understand the genetic basis for the inter-individual variation in the pulmonary vascular response to acute and chronic hypoxia. To date, detailed phenotyping of highlanders has focused on haematocrit and oxygen saturation rather than cardiovascular phenotypes. This review explores what we can learn from those studies with respect to the pulmonary circulation. | en_US |
dc.language.iso | eng | |
dc.publisher | Wiley | |
dc.relation.ispartofseries | British Journal of Dermatology | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es | |
dc.subject | human | en_US |
dc.subject | priority journal | en_US |
dc.subject | genetics | en_US |
dc.subject | altitude | en_US |
dc.subject | arterial smooth muscle cell | en_US |
dc.subject | E1A associated p300 protein | en_US |
dc.subject | endothelin | en_US |
dc.subject | gene identification | en_US |
dc.subject | genetic analysis | en_US |
dc.subject | hematocrit | en_US |
dc.subject | high-altitude | en_US |
dc.subject | homeostasis | en_US |
dc.subject | hypoxia inducible factor | en_US |
dc.subject | hypoxia inducible factor 1alpha | en_US |
dc.subject | hypoxia inducible factor 2alpha | en_US |
dc.subject | hypoxia inducible factor 3alpha | en_US |
dc.subject | hypoxia-induced pulmonary hypertension | en_US |
dc.subject | hypoxia-inducible factor | en_US |
dc.subject | hypoxiainducible factor prolyl hydroxylase 2 | en_US |
dc.subject | interleukin 6 | en_US |
dc.subject | lung artery pressure | en_US |
dc.subject | lung hemodynamics | en_US |
dc.subject | nonhuman | en_US |
dc.subject | oxygen saturation | en_US |
dc.subject | oxygen sensing | en_US |
dc.subject | platelet derived growth factor | en_US |
dc.subject | protein function | en_US |
dc.subject | pulmonary vasoconstriction | en_US |
dc.subject | Review | en_US |
dc.subject | sequence analysis | en_US |
dc.subject | signal transduction | en_US |
dc.subject | vascular remodeling | en_US |
dc.subject | vascular remodelling | en_US |
dc.title | Hypoxia-induced pulmonary hypertension—Utilizing experiments of nature | en_US |
dc.type | info:eu-repo/semantics/review | |
dc.identifier.doi | https://doi.org/10.1111/bph.15144 | |
dc.subject.ocde | https://purl.org/pe-repo/ocde/ford#3.02.15 | |
dc.relation.issn | 1365-2133 |
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