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dc.rights.licenseopenen_US
hal.structure.identifierCentre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] [CRCTB]
dc.contributor.authorROUBENNE, Lukas
hal.structure.identifierCentre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] [CRCTB]
dc.contributor.authorMARTHAN, Roger
dc.contributor.authorLE GRAND, Bruno
hal.structure.identifierCentre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] [CRCTB]
dc.contributor.authorGUIBERT, Christelle
dc.date.accessioned2022-10-12T09:24:54Z
dc.date.available2022-10-12T09:24:54Z
dc.date.issued2021-06-12
dc.identifier.issn2073-4409en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/152322
dc.description.abstractEnPulmonary hypertension (PH) is a severe and multifactorial disease characterized by a progressive elevation of pulmonary arterial resistance and pressure due to remodeling, inflammation, oxidative stress, and vasoreactive alterations of pulmonary arteries (PAs). Currently, the etiology of these pathological features is not clearly understood and, therefore, no curative treatment is available. Since the 1990s, hydrogen sulfide (H2S) has been described as the third gasotransmitter with plethoric regulatory functions in cardiovascular tissues, especially in pulmonary circulation. Alteration in H2S biogenesis has been associated with the hallmarks of PH. H2S is also involved in pulmonary vascular cell homeostasis via the regulation of hypoxia response and mitochondrial bioenergetics, which are critical phenomena affected during the development of PH. In addition, H2S modulates ATP-sensitive K+ channel (KATP) activity, and is associated with PA relaxation. In vitro or in vivo H2S supplementation exerts antioxidative and anti-inflammatory properties, and reduces PA remodeling. Altogether, current findings suggest that H2S promotes protective effects against PH, and could be a relevant target for a new therapeutic strategy, using attractive H2S-releasing molecules. Thus, the present review discusses the involvement and dysregulation of H2S metabolism in pulmonary circulation pathophysiology.
dc.language.isoENen_US
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/
dc.subject.enhydrogen sulfide
dc.subject.enInflammation
dc.subject.enOxidative stress
dc.subject.enPulmonary hypertension
dc.subject.enVascular reactivity
dc.subject.enVascular remodelingH
dc.title.enHydrogen Sulfide Metabolism and Pulmonary Hypertension
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/cells10061477en_US
dc.subject.halSciences de l'ingénieur [physics]en_US
dc.identifier.pubmed34204699en_US
bordeaux.journalCellsen_US
bordeaux.volume10en_US
bordeaux.hal.laboratoriesCentre de Recherche Cardio-Thoracique de Bordeaux (CRCTB) - U 1045en_US
bordeaux.issue6en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-03811881
hal.version1
hal.date.transferred2022-10-12T09:25:03Z
hal.exporttrue
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Cells&rft.date=2021-06-12&rft.volume=10&rft.issue=6&rft.eissn=2073-4409&rft.issn=2073-4409&rft.au=ROUBENNE,%20Lukas&MARTHAN,%20Roger&LE%20GRAND,%20Bruno&GUIBERT,%20Christelle&rft.genre=article


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