Camacho-Pereira 2016 Cell Metab
|Camacho-Pereira J, Tarragó MG, Chini CC, Nin V, Escande C, Warner GM, Puranik AS, Schoon RA, Reid JM, Galina A, Chini EN (2016) CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metab 23:1127-39.|
Abstract: Nicotinamide adenine dinucleotide (NAD) levels decrease during aging and are involved in age-related metabolic decline. To date, the mechanism responsible for the age-related reduction in NAD has not been elucidated. Here we demonstrate 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. We also identified CD38 as the main enzyme involved in the degradation of the NAD precursor nicotinamide mononucleotide (NMN) in vivo, indicating that CD38 has a key role in the modulation of NAD-replacement therapy for aging and metabolic diseases.
Copyright © 2016 Elsevier Inc. All rights reserved. • Keywords: CD38, NAD(+), Aging, Glucose intolerance, Mitochondrial function, Adenocarcinomic human alveolar basal epithelial A549 cells
Labels: MiParea: Respiration, mt-Membrane, mtDNA;mt-genetics, mt-Medicine Pathology: Aging;senescence
Organism: Human, Mouse Tissue;cell: Liver, Lung;gill, Other cell lines Preparation: Intact cells, Isolated mitochondria
Coupling state: LEAK, ROUTINE, OXPHOS, ET Pathway: S, ROX HRR: Oxygraph-2k