CD38通过一种依赖SIRT3的机制决定与年龄相关的NAD下降和线粒体功能障碍。
CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism.
作者信息
Camacho-Pereira Juliana, Tarragó Mariana G, Chini Claudia C S, Nin Veronica, Escande Carlos, Warner Gina M, Puranik Amrutesh S, Schoon Renee A, Reid Joel M, Galina Antonio, Chini Eduardo N
机构信息
Signal Transduction Laboratory, Kogod Aging Center, Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA; Instituto de Bioquímica Médica, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ 21941-590, Brazil.
Signal Transduction Laboratory, Kogod Aging Center, Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
出版信息
Cell Metab. 2016 Jun 14;23(6):1127-1139. doi: 10.1016/j.cmet.2016.05.006.
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.
烟酰胺腺嘌呤二核苷酸（NAD）水平在衰老过程中会下降，并与年龄相关的代谢衰退有关。迄今为止，导致NAD随年龄增长而减少的机制尚未阐明。在此，我们证明了NAD酶CD38的表达和活性随衰老而增加，并且CD38通过至少部分由SIRT3活性调节介导的途径，参与了与年龄相关的NAD下降和线粒体功能障碍。我们还确定CD38是体内参与NAD前体烟酰胺单核苷酸（NMN）降解的主要酶，这表明CD38在调节衰老和代谢疾病的NAD替代疗法中起关键作用。
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