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- _4 wasQuotedFrom 17919258 provenance.
- _4 value "Extensive oxidative and/or nitrosative stress triggers the third pathway by inducing extensive DNA breakage, overactivation of PARP, and consequent depletion of the cellular stores of its substrate NAD+, impairing glycolysis, Krebs cycle, and mitochondrial electron transport, and eventually resulting in ATP depletion and consequent cell dysfunction and death by necrosis. In this case, pharmacological inhibition of PARP or genetic deletion of the PARP-1 preserves cellular NAD+ and ATP pools in oxidatively and/or nitrosatively stressed cardiomyocytes, endothelial or other cell types, thereby allowing them to function normally, or, if the apoptotic process has initiated, to utilize the apoptotic machinery and die by apoptosis instead of necrosis" provenance.