| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8474051 | Journal of Molecular and Cellular Cardiology | 2015 | 11 Pages |
Abstract
Our data suggest that the slow-releasing H2S donor, GYY4137, preserves cardiac function, attenuates adverse remodeling and may exert post-ischemic cardioprotective (pro-angiogenic, anti-apoptotic, anti-hypertrophic and anti-fibrotic) effects in part through enhanced early post-ischemic endogenous natriuretic peptide activation.
Keywords
PRAguanosine 3′5′-cyclic monophosphateP-eNOSLVIDsNPR3NPR1dl-propargylglycineLVEDPLVESVLVEDVLVIDdGYY4137NaHSVEGF-AH2SeNOSBcl-2PAGBNPcGMPANPCSEB-cell CLL/lymphoma 2cystathionine γ-lyaseNPsMyocardial infarctionAngiogenesisRemodelingCardiac outputLeft ventricularLeft ventricular end-diastolic volumeleft ventricular end-systolic volumeintra-peritonealsubcutaneousendothelial nitric oxide synthaseHydrogen sulfidevascular endothelial growth factor-Aleft ventricular end-diastolic pressurePlasma renin activityLADSodium hydrosulfideatrial natriuretic peptideB-type natriuretic peptidenatriuretic peptidesleft anterior descending coronary arteryejection fractionfractional shortening
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Authors
Shera Lilyanna, Meng Teng Peh, Oi Wah Liew, Peipei Wang, Philip K. Moore, Arthur Mark Richards, Eliana C. Martinez,