CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism

Juliana Camacho-Pereira; Mariana G. Tarragó; Claudia C.S. Chini; Veronica Nin; Carlos Escande; Gina M. Warner; Amrutesh S. Puranik; Renee A. Schoon; Joel M. Reid; Antonio Galina; Eduardo N. Chini

doi:10.1016/j.cmet.2016.05.006

CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism

Juliana Camacho-Pereira, Mariana G. Tarragó, Claudia C.S. Chini, Veronica Nin, Carlos Escande, Gina M. Warner, Amrutesh S. Puranik, Renee A. Schoon, Joel M. Reid, Antonio Galina, Eduardo N. Chini

Research output: Contribution to journal › Article

180 Scopus citations

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.

Original language	English (US)
Pages (from-to)	1127-1139
Number of pages	13
Journal	Cell Metabolism
Volume	23
Issue number	6
DOIs	https://doi.org/10.1016/j.cmet.2016.05.006
State	Published - Jun 14 2016

Keywords

CD38
NAD
aging
glucose intolerance
mitochondrial function

ASJC Scopus subject areas

Physiology
Molecular Biology
Cell Biology

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Camacho-Pereira, J., Tarragó, M. G., Chini, C. C. S., Nin, V., Escande, C., Warner, G. M., Puranik, A. S., Schoon, R. A., Reid, J. M., Galina, A., & Chini, E. N. (2016). CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell Metabolism, 23(6), 1127-1139. https://doi.org/10.1016/j.cmet.2016.05.006

CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. / 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.

In: Cell Metabolism, Vol. 23, No. 6, 14.06.2016, p. 1127-1139.

Research output: Contribution to journal › Article

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. / CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. In: Cell Metabolism. 2016 ; Vol. 23, No. 6. pp. 1127-1139.

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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.",

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AU - Escande, Carlos

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AB - 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.

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