Table 1. Occasions of SIRT1 – PARP interaction in oxidative stress-related pathologies.

Organ system	Disease	Partners	Models	Mechanism	Effect	Ref.
Cardiovascular system	Angiotensin-induced cardiac hypertrophy	PARP-1 SIRT1	PARP-1−/− mice, primary cardiomyocytes treated with resveratrol, SIRT1 siRNA, or by SIRT1 overexpression.	PARP-1 activation inhibits SIRT1 through NAD+ depletion.	Both SIRT1 activation and PARP inhibition protect against angiotensin II-mediated and oxidant-mediated cardiomyocyte cell death.	(Pillai, et al. 2006.)
	Heart failure (aortic banding model)	PARP-1 SIRT1	Cardiomyocytes overexpressing PARP-1, SIRT1, or treated with resveratrol, sirtinol, SIRT1 siRNA	PARP-1 limits NAD+ levels and hence SIRT1 activity through limiting NAD+ for SIRT1 action and probably by repressing SIRT1 expression.	SIRT1 induction protect against oxidant-induced cardiomyocytes cell death.	(Pillai, et al. 2005.)
	Shear stress on endothelial cells	PARP-1 SIRT1	HUVEC cells undergoing shear stress treated with ABT888 and PARP-1 siRNA	Shear stress decrease NAD+ levels, SIRT1 activity and expression that is reverted by PARP-1 depletion, or inhibition.	Proinflammatory conditions and cell death provoked by shear stress is reduced.	(Qin, et al. 2012.)
	DOX-induced vascular damage	PARP-2 SIRT1	PARP-2 knockout mice and PARP-2 knockdown MOVAS cells	SIRT1 promoter is released from suppression upon PARP-2 depletion that induces mitochondrial biogenesis.	Vascular protection against DOX damage upon SIRT1 induction after PARP-2 depletion.	(Szanto, et al. 2011.)
Central nervous system	Trophic deprivation and oxidant mediated neuronal cell death	PARP-1 SIRT1	Near-pure cortical neuronal cell cultures from PARP-1−/− mice. Same neurons treated with fisetin, resveratrol and sirtinol.	PARP-1 activation inhibits SIRT1 through NAD+ depletion. Protective effect of SIRT1 activation is not explained.	Both SIRT1 activation and PARP inhibition protect against neurotoxicity.	(Sheline, et al. 2010.)
	Glutamate/NMDA neurotoxicity	PARP-1 SIRT1	Dissociated cerebral cortical cell cultures from embryonic rat treated with sirtinol and resveratrol.	NMDA treatment reduces SIRT1 activation probably due to PARP activation and NAD+ depletion. Protective effect of SIRT1 activation is not explained.	Reduction of cell death upon SIRT1 activation and PARP inhibition.	(Liu, et al. 2008.) (Liu, et al. 2009.)
Gastrointestinal tract	Glucose toxicity on hepatocytes	PARP-1 SIRT1	HepG2 cells treated with PJ34 and PARP-1 siRNA.	PARP-1 activation decreases SIRT1 activity that is restored by PARP inhibition probably through conservation of NAD+ levels.	Glucose toxicity is reverted by PARP inhibition.	(Pang, et al. 2011.)

Abbreviations in text.

Fistein and resveratrol are SIRT1 activators, sirtinol is a SIRT1 inhibitor, 3-amino-benzamide (3AB) and PJ34 are PARP inhibitors.