Diabetic endothelial dysfunction: the role of poly(ADP-ribose) polymerase activation

By F. Soriano, László Virág, P. Jagtap, É. Szabó, J. Mabley, L. Liaudet, A. Marton, D. Hoyt, K. Murthy, A. Salzman and 2 more. Nature Medicine, 2001

630 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Endocrinology, Diabetes and Metabolism

View Paper: https://www.semanticscholar.org/paper/1060bedc5b56b0b2d12b62944cb9f07edbafe6d4

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In Clinical Biochemistry

M. Brownlee

In Endocrinology, Diabetes and Metabolism

Citations in the corpus

Age Related Changes in NAD+ Metabolism Oxidative Stress and Sirt1 Activity in Wistar Rats (2011, background): “In these diseases, the oxidantmediated endothelial cell injury is dependent on PARP activation, and can be attenuated by pharmacological PARP inhibitors [25,26].”
Endothelial dysfunction in diabetes mellitus (2007, neutral): “Treatment with a novel potent PARP inhibitor, starting after the time of islet destruction, maintained normal vascular responsiveness, despite the persistence of severe hyperglycemia (Garcia Soriano et al 2001).”
New insights on oxidative stress and diabetic complications may lead to a "causal" antioxidant therapy. (2003, background): “PEROXYNITRITE, DNA DAMAGE, AND ENDOTHELIAL DYSFUNCTION: THE ROLE OF POLY(ADP-RIBOSE) POLYMERASE ACTIVATION — Peroxynitrite is a potent initiator of DNA single-strand breakage, which is an obligatory stimulus for the activation of the nuclear enzyme poly(ADP-ribose) polymerase (48).”
Endothelial dysfunction - a major mediator of diabetic vascular disease. (2013, background): “Furthermore, chronic treatment with the PARP inhibitors in rodent models has been demonstrated to improve endothelial dysfunction associated with aging [195,197].”
Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. (2003, methodology): “For in vivo immunoprecipitated Western blots, thoracic aortas from WT and PARP-deficient mice were incubated exactly as described in (10).”
The Therapeutic Potential of Poly(ADP-Ribose) Polymerase Inhibitors (2002, background): “Similarly, PJ34 exerts marked protective effects against the histological damage, lipid peroxidation, neutrophil infiltration, and mortality in a dextrane sulfate colitis model in the mouse (Mabley et al., 2001a).”
PARP-1 inhibition increases mitochondrial metabolism through SIRT1 activation (2011, positive): “Interestingly, the inhibition of PARP activity with PJ34 (Garcia Soriano et al., 2001) rescued the drop in NAD+ and recovered SIRT1 function during H2O2 exposure (Figures 4B–4D).”
Vascular complications of diabetes: mechanisms of injury and protective factors (2013, background): “By promoting DNA strand breaks, oxidative stress can activate PARP, which in turn can activate NFkB and cause endothelial dysfunction (Garcia Soriano et al., 2001).”