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When a low dose of aspirin is administered orally (most commonly 81 mg), its context-sensitive drug disposition via the portal circulation combined with the difference in IC50 values for COX-1 vs COX-2 both contribute significantly to the high selectivity by which low dose oral aspirin inhibits platelet COX-1 vs other COX-2 found in other nucleated tissues such as the vascular endothelium (Pedersen & FitzGerald, 1984

Despite their proliferative arrest, senescent cells exhibit a metabolically active state characterized by an altered glycolytic flux, perturbed lipid homeostasis, mitochondrial dysfunction, and a disrupted nicotinamide adenine dinucleotide (NAD +) redox balance, all of which contribute to vascular damage

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