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Hydrogen sulfide cytoprotective signaling is endothelial nitric oxide synthase-nitric oxide dependent
TLDR
The results suggest that H2S-mediated cytoprotective signaling in the setting of I/R injury is dependent in large part on eNOS activation and NO generation, and indicates that hydrogen sulfide protects against multiple cardiovascular disease states in a similar manner as nitric oxide. Expand
H2S Protects Against Pressure Overload–Induced Heart Failure via Upregulation of Endothelial Nitric Oxide Synthase
TLDR
H2S levels are decreased in mice in the setting of heart failure, and oral H2S therapy prevents the transition from compensated to decompensated heart failure in part via upregulation of endothelial nitric oxide synthase and increased Nitric oxide bioavailability. Expand
Exercise Protects Against Myocardial Ischemia–Reperfusion Injury via Stimulation of &bgr;3-Adrenergic Receptors and Increased Nitric Oxide Signaling: Role of Nitrite and Nitrosothiols
TLDR
Findings clearly demonstrate that exercise protects the heart against myocardial ischemia–reperfusion injury by stimulation of &bgr;3-ARs and increased cardiac storage of nitric oxide metabolites (ie, nitrite and nitrosothiols). Expand
Genetic and Pharmacologic Hydrogen Sulfide Therapy Attenuates Ischemia-Induced Heart Failure in Mice
TLDR
Exogenous H2S therapy administered at the time of reperfusion and then daily for the first 7 days after myocardial ischemia also protected against the structural and functional deterioration of the left ventricle by attenuating oxidative stress and mitochondrial dysfunction. Expand
Hydrogen sulfide preconditions the db/db diabetic mouse heart against ischemia-reperfusion injury by activating Nrf2 signaling in an Erk-dependent manner.
TLDR
It is demonstrated for the first time that exogenous administration of Na2S attenuates myocardial ischemia-reperfusion injury in db/db mice, suggesting the potential therapeutic effects of H2S in treating a heart attack in the setting of type 2 diabetes. Expand
DJ-1 protects the heart against ischemia-reperfusion injury by regulating mitochondrial fission.
TLDR
The data demonstrates that the activation of DJ-1 in response to myocardial I/R injury protects the heart by regulating the SUMOylation status of Drp1 and attenuating excessive mitochondrial fission. Expand
Hydrogen sulfide attenuates high fat diet-induced cardiac dysfunction via the suppression of endoplasmic reticulum stress.
TLDR
Evaluation of circulating and cardiac H2S levels in a murine model of high fat diet (HFD)-induced cardiomyopathy suggests that diminished circulating and heart rate levels play a role in the pathophysiology of HFD-induced carduomyopathy, and suggests that H 2S therapy may be of clinical importance in the treatment of cardiovascular complications stemming from diabetes. Expand
Hydrogen sulfide and ischemia-reperfusion injury.
TLDR
The role H(2)S plays in different model systems of I/R injury is described and some of the mechanisms involved with its cytoprotection are detailed. Expand
Nitrite Therapy Improves Left Ventricular Function During Heart Failure via Restoration of Nitric Oxide–Mediated Cytoprotective Signaling
TLDR
The emerging concept that nitrite therapy may be a viable clinical option for increasing NO levels and may have a practical clinical use in the treatment of heart failure is supported. Expand
Hydrogen sulfide provides cardioprotection against myocardial/ischemia reperfusion injury in the diabetic state through the activation of the RISK pathway
TLDR
Findings provide important information that myocardial Erk1/2 activation by Na2S therapy following MI/R sets into motion events, which ultimately lead to cardioprotection in the setting of diabetes. Expand
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