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Phosphodiesterase-5 Inhibitor Sildenafil Preconditions Adult Cardiac Myocytes against Necrosis and Apoptosis
TLDR
The data provide strong evidence for a direct protective effect of sildenafil against necrosis and apoptosis through NO signaling pathway and may have possible therapeutic potential in preventing myocyte cell death following ischemia/reperfusion.
The oxygen free radical system: from equations through membrane-protein interactions to cardiovascular injury and protection.
TLDR
This thesis highlights several novel therapeutic strategies aimed at interrupting the oxygen free radical mediated component of ischaemia/reperfusion injury and points out and emphasises the growing importance of the role of singlet oxygen.
HIF-1 activation attenuates postischemic myocardial injury: role for heme oxygenase-1 in modulating microvascular chemokine generation.
TLDR
The data show that HIF-1 activation induces substantial HO-1 expression that is associated with attenuated proinflammatory chemokine production by microvascular endothelium in vitro and in vivo.
PGH Synthase and Lipoxygenase Generate Superoxide in the Presence of NADH or NADPH
TLDR
It is concluded that PGH synthase and lipoxygenase produce superoxide via a side-chain reaction dependent on the presence of suitable reducing cosubstrate, analogous to that described for peroxidases in general.
Sildenafil (Viagra) induces powerful cardioprotective effect via opening of mitochondrial K(ATP) channels in rabbits.
TLDR
For the first time, it is demonstrated that sildenafil induces acute and delayed protective effects against ischemia-reperfusion injury, which are mediated by opening of mitochondrial K(ATP) channels.
Cardioprotection with phosphodiesterase-5 inhibition--a novel preconditioning strategy.
A Novel Role of MicroRNA in Late Preconditioning: Upregulation of Endothelial Nitric Oxide Synthase and Heat Shock Protein 70
TLDR
It is concluded that IPC-induced miRNAs trigger cardioprotection similar to the delayed phase of IPC, possibly through upregulating eNOS, HSP70, and the HSP 70 transcription factor HSF-1.
Cobalt chloride induces delayed cardiac preconditioning in mice through selective activation of HIF-1alpha and AP-1 and iNOS signaling.
TLDR
It is concluded that in vivo administration of CoCl2 preconditions the heart against I/R injury and is achieved through a distinctive signaling mechanism involving HIF-1alpha, AP-1, and iNOS but independent of NF-kappaB activation.
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