Veronica Nin

TL;DR: It is demonstrated that expression and activity of the NADase CD38 increase with aging and that CD38 is required for the age-related NAD decline and mitochondrial dysfunction via a pathway mediated at least in part by regulation of SIRT3 activity.

TL;DR: The results show that CD38 is a novel pharmacological target to treat metabolic diseases via NAD+-dependent pathways and that pharmacological inhibition of CD38 results in higher intracellular NAD+ levels and that treatment of cell cultures with apigenin decreases global acetylation as well as theacetylation of p53 and RelA-p65.

TL;DR: It is proposed that the DBC1-SIRT1 interaction may serve as a new target for therapies aimed at nonalcoholic liver steatosis and what is believed to be a new role for DBC 1 as an in vivo regulator of SIRT1 activity and liver Steatosis.

TL;DR: It is demonstrated that NAD metabolism is essential for pancreatic cancer cell survival and proliferation and that targeting NAD synthesis via the Nampt pathway could lead to novel therapeutic treatments for Pancreatic cancer.

TL;DR: It is shown that food restriction (FR) effectively slows the course of the disease in mouse models of ADPKD and suggests that dietary interventions such as FR, or treatment that mimics the effects of such interventions, may be potential and novel preventive and therapeutic options for patients with AD PKD.