Does nuclear factor-kappaB repress hypoxia-induced mitochondrial defects and cell death of ventricular myocytes?
To the best of our knowledge, the data provide the first direct evidence that activation of the NF-kappaB signaling pathways is sufficient to suppress cell death of ventricular myocytes during hypoxia. Moreover, our data further suggest that NF-kappaB averts cell death through a mechanism that prevents perturbations to the mitochondrion during hypoxic injury.
Addition of an iron chelator to the preservation solution UW did not improve kidney function after both CS and CP. Iron chelation is not able to prevent cold-induced damage in the isolated perfused rat kidney.