Given that AMPK activity is inhibited under hyperglycemia and a high level of Ang II, both known to augment oxidative stress in ECs [21,22], we first sought to test whether phosphorylation of PARP1 Ser-177 was also decreased under these conditions with the use of the newly developed anti-phospho-PARP1. The gene discussed is PRKAA1; the disease is Hyperglycemia.