Matches in SemOpenAlex for { <https://semopenalex.org/work/W3110012469> ?p ?o ?g. }
- W3110012469 endingPage "101817" @default.
- W3110012469 startingPage "101817" @default.
- W3110012469 abstract "Oxidative stress drives the pathogenesis of atrial fibrillation (AF), the most common arrhythmia. In the cardiovascular system, cystathionine γ-lyase (CSE) serves as the primary enzyme producing hydrogen sulfide (H2S), a mammalian gasotransmitter that reduces oxidative stress. Using a case control study design in patients with and without AF and a mouse model of CSE knockout (CSE-KO), we evaluated the role of H2S in the etiology of AF. Patients with AF (n = 51) had significantly reduced plasma acid labile sulfide levels compared to patients without AF (n = 65). In addition, patients with persistent AF (n = 25) showed lower plasma free sulfide levels compared to patients with paroxysmal AF (n = 26). Consistent with an important role for H2S in AF, CSE-KO mice had decreased atrial sulfide levels, increased atrial superoxide levels, and enhanced propensity for induced persistent AF compared to wild type (WT) mice. Rescuing H2S signaling in CSE-KO mice by Diallyl trisulfide (DATS) supplementation or reconstitution with endothelial cell specific CSE over-expression significantly reduced atrial superoxide, increased sulfide levels, and lowered AF inducibility. Lastly, low H2S levels in CSE KO mice was associated with atrial electrical remodeling including longer effective refractory periods, slower conduction velocity, increased myocyte calcium sparks, and increased myocyte action potential duration that were reversed by DATS supplementation or endothelial CSE overexpression. Our findings demonstrate an important role of CSE and H2S bioavailability in regulating electrical remodeling and susceptibility to AF." @default.
- W3110012469 created "2020-12-07" @default.
- W3110012469 creator A5009347189 @default.
- W3110012469 creator A5012681244 @default.
- W3110012469 creator A5013485864 @default.
- W3110012469 creator A5024890460 @default.
- W3110012469 creator A5027084053 @default.
- W3110012469 creator A5028646111 @default.
- W3110012469 creator A5039853523 @default.
- W3110012469 creator A5042359264 @default.
- W3110012469 creator A5044661473 @default.
- W3110012469 creator A5054465625 @default.
- W3110012469 creator A5060458446 @default.
- W3110012469 creator A5065863693 @default.
- W3110012469 creator A5067696537 @default.
- W3110012469 creator A5069796229 @default.
- W3110012469 creator A5090639896 @default.
- W3110012469 creator A5091105956 @default.
- W3110012469 date "2021-01-01" @default.
- W3110012469 modified "2023-10-02" @default.
- W3110012469 title "Decreased bioavailability of hydrogen sulfide links vascular endothelium and atrial remodeling in atrial fibrillation" @default.
- W3110012469 cites W1470476341 @default.
- W3110012469 cites W1592150753 @default.
- W3110012469 cites W1968825092 @default.
- W3110012469 cites W1970863922 @default.
- W3110012469 cites W1979710206 @default.
- W3110012469 cites W1992890855 @default.
- W3110012469 cites W1994456301 @default.
- W3110012469 cites W1998183255 @default.
- W3110012469 cites W2003861270 @default.
- W3110012469 cites W2004497484 @default.
- W3110012469 cites W2012571321 @default.
- W3110012469 cites W2018761453 @default.
- W3110012469 cites W2020599071 @default.
- W3110012469 cites W2031257150 @default.
- W3110012469 cites W2071146637 @default.
- W3110012469 cites W2075062016 @default.
- W3110012469 cites W2088612590 @default.
- W3110012469 cites W2092709589 @default.
- W3110012469 cites W2093553238 @default.
- W3110012469 cites W2108375254 @default.
- W3110012469 cites W2109825385 @default.
- W3110012469 cites W2117941518 @default.
- W3110012469 cites W2118554426 @default.
- W3110012469 cites W2120464741 @default.
- W3110012469 cites W2122199958 @default.
- W3110012469 cites W2134743654 @default.
- W3110012469 cites W2153043966 @default.
- W3110012469 cites W2155871460 @default.
- W3110012469 cites W2159789451 @default.
- W3110012469 cites W2161903254 @default.
- W3110012469 cites W2170737858 @default.
- W3110012469 cites W2171992151 @default.
- W3110012469 cites W2327269495 @default.
- W3110012469 cites W2392200964 @default.
- W3110012469 cites W2565597194 @default.
- W3110012469 cites W2567697352 @default.
- W3110012469 cites W2606655364 @default.
- W3110012469 cites W2741602250 @default.
- W3110012469 cites W2742923212 @default.
- W3110012469 cites W2785842418 @default.
- W3110012469 cites W2792880935 @default.
- W3110012469 cites W2888580420 @default.
- W3110012469 cites W2899497612 @default.
- W3110012469 cites W2913705661 @default.
- W3110012469 cites W2951906113 @default.
- W3110012469 cites W2997346889 @default.
- W3110012469 cites W3004217996 @default.
- W3110012469 cites W3009846732 @default.
- W3110012469 cites W3017367409 @default.
- W3110012469 cites W4376489815 @default.
- W3110012469 doi "https://doi.org/10.1016/j.redox.2020.101817" @default.
- W3110012469 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7732878" @default.
- W3110012469 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33310503" @default.
- W3110012469 hasPublicationYear "2021" @default.
- W3110012469 type Work @default.
- W3110012469 sameAs 3110012469 @default.
- W3110012469 citedByCount "15" @default.
- W3110012469 countsByYear W31100124692021 @default.
- W3110012469 countsByYear W31100124692022 @default.
- W3110012469 countsByYear W31100124692023 @default.
- W3110012469 crossrefType "journal-article" @default.
- W3110012469 hasAuthorship W3110012469A5009347189 @default.
- W3110012469 hasAuthorship W3110012469A5012681244 @default.
- W3110012469 hasAuthorship W3110012469A5013485864 @default.
- W3110012469 hasAuthorship W3110012469A5024890460 @default.
- W3110012469 hasAuthorship W3110012469A5027084053 @default.
- W3110012469 hasAuthorship W3110012469A5028646111 @default.
- W3110012469 hasAuthorship W3110012469A5039853523 @default.
- W3110012469 hasAuthorship W3110012469A5042359264 @default.
- W3110012469 hasAuthorship W3110012469A5044661473 @default.
- W3110012469 hasAuthorship W3110012469A5054465625 @default.
- W3110012469 hasAuthorship W3110012469A5060458446 @default.
- W3110012469 hasAuthorship W3110012469A5065863693 @default.
- W3110012469 hasAuthorship W3110012469A5067696537 @default.
- W3110012469 hasAuthorship W3110012469A5069796229 @default.
- W3110012469 hasAuthorship W3110012469A5090639896 @default.
- W3110012469 hasAuthorship W3110012469A5091105956 @default.