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The role of H2S bioavailability in endothelial dysfunction

dc.contributor.authorWang, R
dc.contributor.authorSzabo, C
dc.contributor.authorIchinose, F
dc.contributor.authorAhmed, A
dc.contributor.authorWhiteman, M
dc.contributor.authorPapapetropoulos, A
dc.date.accessioned2016-09-05T13:01:06Z
dc.date.issued2015-06-09
dc.description.abstractEndothelial dysfunction (EDF) reflects pathophysiological changes in the phenotype and functions of endothelial cells that result from and/or contribute to a plethora of cardiovascular diseases. We review the role of hydrogen sulfide (H2S) in the pathogenesis of EDF, one of the fastest advancing research topics. Conventionally treated as an environment pollutant, H2S is also produced in endothelial cells and participates in the fine regulation of endothelial integrity and functions. Disturbed H2S bioavailability has been suggested to be a novel indicator of EDF progress and prognosis. EDF manifests in different forms in multiple pathologies, but therapeutics aimed at remedying altered H2S bioavailability may benefit all.en_GB
dc.description.sponsorshipThis work has been supported by a Discovery Grant from Natural Sciences and Engineering Research council of Canada to RW. CS has been supported by the American Diabetes Association, the National Institutes of Health of USA and the Shriners Hospitals for Children. FI has been supported by the National Institutes of Health of USA. MW has been supported by the Medical Research Council of UK. AA has been supported by programme grants from British Heart Foundation (RG/09/001/25940), Medical Research Council (G0700288), Royal Society and European Union. AP has been supported through an Aristeia grant (1436) that is co-financed by the European Union (ESF) and Greek national funds through the Operational Program “Education and Lifelong Learning”. MW and AP are supported by the COST Action BM1005 (ENOG: European network on gasotransmitters).en_GB
dc.identifier.citationVol. 36, pp. 568 - 578en_GB
dc.identifier.doi10.1016/j.tips.2015.05.007
dc.identifier.otherS0165-6147(15)00097-8
dc.identifier.urihttp://hdl.handle.net/10871/23301
dc.language.isoenen_GB
dc.publisherElsevieren_GB
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/26071118en_GB
dc.subjectcystathionine gamma-lyaseen_GB
dc.subjectendothelium-derived hyperpolarizing factoren_GB
dc.subjectgasotransmittersen_GB
dc.subjectheme oxygenase-1en_GB
dc.subjecthydrogen sulfideen_GB
dc.subjectnitric oxideen_GB
dc.subjectAnimalsen_GB
dc.subjectEndothelium, Vascularen_GB
dc.subjectFree Radicalsen_GB
dc.subjectHumansen_GB
dc.subjectHydrogen Sulfideen_GB
dc.subjectVascular Diseasesen_GB
dc.titleThe role of H2S bioavailability in endothelial dysfunctionen_GB
dc.typeArticleen_GB
dc.date.available2016-09-05T13:01:06Z
dc.identifier.issn0165-6147
exeter.place-of-publicationEnglanden_GB
dc.descriptionThis is the author accepted manuscript. The final version is available from the publisher via the DOI in this record.en_GB
dc.identifier.journalTrends in Pharmacological Sciencesen_GB
dc.identifier.pmcidPMC4562801
dc.identifier.pmid26071118


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