2008
DOI: 10.1152/ajpheart.00244.2008
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Endogenous hydrogen sulphide mediates the cardioprotection induced by ischemic postconditioning

Abstract: Yong QC, Lee SW, Foo CS, Neo KL, Chen X, Bian JS. Endogenous hydrogen sulphide mediates the cardioprotection induced by ischemic postconditioning.

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Cited by 117 publications
(128 citation statements)
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References 61 publications
(88 reference statements)
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“…Importantly, both endogenous and exogenous H 2 S induce PostC-like cardioprotection, involving the Akt-eNOS-PKC pathway. Moreover, the PKC inhibitor chelerythrine and the K ATP channel blockers, glibenclamide or 5-hydroxydecanoate, are able to reverse the cardioprotective effects of the H 2 S-donor, NaHS (89,203). While it is not clear whether and=or how H 2 S modifies the activity of RISK=SAFE enzymes involved in PostC, it seems that H 2 S directly alters the activity of K ATP channels.…”
Section: S-sulfhydrationmentioning
confidence: 99%
“…Importantly, both endogenous and exogenous H 2 S induce PostC-like cardioprotection, involving the Akt-eNOS-PKC pathway. Moreover, the PKC inhibitor chelerythrine and the K ATP channel blockers, glibenclamide or 5-hydroxydecanoate, are able to reverse the cardioprotective effects of the H 2 S-donor, NaHS (89,203). While it is not clear whether and=or how H 2 S modifies the activity of RISK=SAFE enzymes involved in PostC, it seems that H 2 S directly alters the activity of K ATP channels.…”
Section: S-sulfhydrationmentioning
confidence: 99%
“…Together with other groups, we have found that both endogenous and exogenous H 2 S protect the heart from isoproterenol-induced myocardial injury by directly scavenging oxygen free radicals (Geng et al, 2004a) and inhibiting the adenylyl cyclase/ cAMP pathway or L-type calcium channel (Yong et al, 2008b). Moreover, researchers have found that preconditioning and postconditioning with H 2 S produced cardioprotective effects against ischemic injury via the regulation of protein kinase C, K ATP channels, cyclooxygenase-2, NO, p42/44-mitogen-activated protein kinase, phosphoinositol-3-kinase (PI3K)/Akt, and GSK3␤ pathways Yong et al, 2008a;Yao et al, 2010). More importantly, endogenous H 2 S was found to contribute to the cardioprotection induced by ischemic preconditioning and postconditioning Pan et al, 2006;Yong et al, 2008a).…”
Section: Introductionmentioning
confidence: 99%
“…Moreover, researchers have found that preconditioning and postconditioning with H 2 S produced cardioprotective effects against ischemic injury via the regulation of protein kinase C, K ATP channels, cyclooxygenase-2, NO, p42/44-mitogen-activated protein kinase, phosphoinositol-3-kinase (PI3K)/Akt, and GSK3␤ pathways Yong et al, 2008a;Yao et al, 2010). More importantly, endogenous H 2 S was found to contribute to the cardioprotection induced by ischemic preconditioning and postconditioning Pan et al, 2006;Yong et al, 2008a). In addition, H 2 S may produce a proangiogenic effect (Cai et al, 2007) that can contribute to its cardioprotective action.…”
Section: Introductionmentioning
confidence: 99%
“…there may be reduced H 2 S production (Yong et al, 2008, Han et al, 2015, Islam et 109 al., 2015. The administration of exogenous H 2 S donor compounds or increasing 110 endogenous production of H 2 S has been well documented to reduce ischemia-…”
mentioning
confidence: 99%