NAD and the aging process: Role in life, death and everything in between

Life as we know it cannot exist without the nucleotide nicotinamide adenine dinucleotide (NAD). From the simplest organism, such as bacteria, to the most complex multicellular organisms, NAD is a key cellular component. NAD is extremely abundant in most living cells and has traditionally been descri...

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Published inMolecular and cellular endocrinology Vol. 455; pp. 62 - 74
Main Authors Chini, Claudia C.S., Tarragó, Mariana G., Chini, Eduardo N.
Format Journal Article
LanguageEnglish
Published Ireland Elsevier B.V 05.11.2017
Subjects
ADP-ribosyl Cyclase 1 - genetics
ADP-ribosyl Cyclase 1 - metabolism
Aging
Aging - genetics
Aging - metabolism
Animals
Armadillo Domain Proteins - genetics
Armadillo Domain Proteins - metabolism
bacteria
calcium
Caloric Restriction
CD38
chromatin
Cyclic ADP-Ribose - metabolism
Cytoskeletal Proteins - genetics
Cytoskeletal Proteins - metabolism
death
electron transfer
epigenetics
Humans
Membrane Glycoproteins - genetics
Membrane Glycoproteins - metabolism
metabolism
Mitochondria - genetics
Mitochondria - metabolism
Mitochondrial function
NAD
NAD (coenzyme)
NAD - metabolism
NADP - analogs & derivatives
NADP - metabolism
Oxidation-Reduction
PARP
Poly(ADP-ribose) Polymerases - genetics
Poly(ADP-ribose) Polymerases - metabolism
Protein Processing, Post-Translational
Signal Transduction
SIRTUINS
Sirtuins - genetics
Sirtuins - metabolism
NAD
Aging
CD38
PARP
SIRTUINS
Mitochondrial function
NAD(+)
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Abstract Life as we know it cannot exist without the nucleotide nicotinamide adenine dinucleotide (NAD). From the simplest organism, such as bacteria, to the most complex multicellular organisms, NAD is a key cellular component. NAD is extremely abundant in most living cells and has traditionally been described to be a cofactor in electron transfer during oxidation-reduction reactions. In addition to participating in these reactions, NAD has also been shown to play a key role in cell signaling, regulating several pathways from intracellular calcium transients to the epigenetic status of chromatin. Thus, NAD is a molecule that provides an important link between signaling and metabolism, and serves as a key molecule in cellular metabolic sensoring pathways. Importantly, it has now been clearly demonstrated that cellular NAD levels decline during chronological aging. This decline appears to play a crucial role in the development of metabolic dysfunction and age-related diseases. In this review we will discuss the molecular mechanisms responsible for the decrease in NAD levels during aging. Since other reviews on this subject have been recently published, we will concentrate on presenting a critical appraisal of the current status of the literature and will highlight some controversial topics in the field. In particular, we will discuss the potential role of the NADase CD38 as a driver of age-related NAD decline. •NAD plays a key role in energy metabolism, cell signaling and energy sensing.•Cellular NAD levels decrease during the process of chronological aging.•NAD decline during aging leads to decrease in SIRTUINS activity, mitochondrial and metabolic dysfunction.•The enzyme CD38 is the main NADase in tissues and plays a key role on the age-related NAD decline.•NAD replacement therapy may serve as target for age-related metabolic dysfunction.
AbstractList Life as we know it cannot exist without the nucleotide nicotinamide adenine dinucleotide (NAD). From the simplest organism, such as bacteria, to the most complex multicellular organisms, NAD is a key cellular component. NAD is extremely abundant in most living cells and has traditionally been described to be a cofactor in electron transfer during oxidation-reduction reactions. In addition to participating in these reactions, NAD has also been shown to play a key role in cell signaling, regulating several pathways from intracellular calcium transients to the epigenetic status of chromatin. Thus, NAD is a molecule that provides an important link between signaling and metabolism, and serves as a key molecule in cellular metabolic sensoring pathways. Importantly, it has now been clearly demonstrated that cellular NAD levels decline during chronological aging. This decline appears to play a crucial role in the development of metabolic dysfunction and age-related diseases. In this review we will discuss the molecular mechanisms responsible for the decrease in NAD levels during aging. Since other reviews on this subject have been recently published, we will concentrate on presenting a critical appraisal of the current status of the literature and will highlight some controversial topics in the field. In particular, we will discuss the potential role of the NADase CD38 as a driver of age-related NAD decline.Life as we know it cannot exist without the nucleotide nicotinamide adenine dinucleotide (NAD). From the simplest organism, such as bacteria, to the most complex multicellular organisms, NAD is a key cellular component. NAD is extremely abundant in most living cells and has traditionally been described to be a cofactor in electron transfer during oxidation-reduction reactions. In addition to participating in these reactions, NAD has also been shown to play a key role in cell signaling, regulating several pathways from intracellular calcium transients to the epigenetic status of chromatin. Thus, NAD is a molecule that provides an important link between signaling and metabolism, and serves as a key molecule in cellular metabolic sensoring pathways. Importantly, it has now been clearly demonstrated that cellular NAD levels decline during chronological aging. This decline appears to play a crucial role in the development of metabolic dysfunction and age-related diseases. In this review we will discuss the molecular mechanisms responsible for the decrease in NAD levels during aging. Since other reviews on this subject have been recently published, we will concentrate on presenting a critical appraisal of the current status of the literature and will highlight some controversial topics in the field. In particular, we will discuss the potential role of the NADase CD38 as a driver of age-related NAD decline.
Life as we know it cannot exist without the nucleotide nicotinamide adenine dinucleotide (NAD). From the simplest organism, such as bacteria, to the most complex multicellular organisms, NAD is a key cellular component. NAD is extremely abundant in most living cells and has traditionally been described to be a cofactor in electron transfer during oxidation-reduction reactions. In addition to participating in these reactions, NAD has also been shown to play a key role in cell signaling, regulating several pathways from intracellular calcium transients to the epigenetic status of chromatin. Thus, NAD is a molecule that provides an important link between signaling and metabolism, and serves as a key molecule in cellular metabolic sensoring pathways. Importantly, it has now been clearly demonstrated that cellular NAD levels decline during chronological aging. This decline appears to play a crucial role in the development of metabolic dysfunction and age-related diseases. In this review we will discuss the molecular mechanisms responsible for the decrease in NAD levels during aging. Since other reviews on this subject have been recently published, we will concentrate on presenting a critical appraisal of the current status of the literature and will highlight some controversial topics in the field. In particular, we will discuss the potential role of the NADase CD38 as a driver of age-related NAD decline.
Life as we know it cannot exist without the nucleotide nicotinamide adenine dinucleotide (NAD). From the simplest organism, such as bacteria, to the most complex multicellular organisms, NAD is a key cellular component. NAD is extremely abundant in most living cells and has traditionally been described to be a cofactor in electron transfer during oxidation-reduction reactions. In addition to participating in these reactions, NAD has also been shown to play a key role in cell signaling, regulating several pathways from intracellular calcium transients to the epigenetic status of chromatin. Thus, NAD is a molecule that provides an important link between signaling and metabolism, and serves as a key molecule in cellular metabolic sensoring pathways. Importantly, it has now been clearly demonstrated that cellular NAD levels decline during chronological aging. This decline appears to play a crucial role in the development of metabolic dysfunction and age-related diseases. In this review we will discuss the molecular mechanisms responsible for the decrease in NAD levels during aging. Since other reviews on this subject have been recently published, we will concentrate on presenting a critical appraisal of the current status of the literature and will highlight some controversial topics in the field. In particular, we will discuss the potential role of the NADase CD38 as a driver of age-related NAD decline. •NAD plays a key role in energy metabolism, cell signaling and energy sensing.•Cellular NAD levels decrease during the process of chronological aging.•NAD decline during aging leads to decrease in SIRTUINS activity, mitochondrial and metabolic dysfunction.•The enzyme CD38 is the main NADase in tissues and plays a key role on the age-related NAD decline.•NAD replacement therapy may serve as target for age-related metabolic dysfunction.
Author Chini, Claudia C.S.
Chini, Eduardo N.
Tarragó, Mariana G.
AuthorAffiliation a Signal Transduction Laboratory. Kogod Aging Center, Department of Anesthesiology, Oncology Research, GI signaling center, Mayo Clinic College of Medicine, Rochester, Minnesota 55905
AuthorAffiliation_xml – name: a Signal Transduction Laboratory. Kogod Aging Center, Department of Anesthesiology, Oncology Research, GI signaling center, Mayo Clinic College of Medicine, Rochester, Minnesota 55905
Author_xml – sequence: 1
  givenname: Claudia C.S.
  surname: Chini
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  givenname: Eduardo N.
  surname: Chini
  fullname: Chini, Eduardo N.
  email: chini.eduardo@mayo.edu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27825999$$D View this record in MEDLINE/PubMed
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IngestDate Thu Aug 21 14:32:27 EDT 2025
Mon Jul 21 11:11:32 EDT 2025
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Thu Apr 03 07:01:42 EDT 2025
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Thu Jul 03 08:17:46 EDT 2025
Fri Feb 23 02:20:40 EST 2024
IsPeerReviewed true
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Keywords NAD
Aging
CD38
PARP
SIRTUINS
Mitochondrial function
NAD(+)
Language English
License Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.
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PublicationTitle Molecular and cellular endocrinology
PublicationTitleAlternate Mol Cell Endocrinol
PublicationYear 2017
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Snippet Life as we know it cannot exist without the nucleotide nicotinamide adenine dinucleotide (NAD). From the simplest organism, such as bacteria, to the most...
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SubjectTerms ADP-ribosyl Cyclase 1 - genetics
ADP-ribosyl Cyclase 1 - metabolism
Aging
Aging - genetics
Aging - metabolism
Animals
Armadillo Domain Proteins - genetics
Armadillo Domain Proteins - metabolism
bacteria
calcium
Caloric Restriction
CD38
chromatin
Cyclic ADP-Ribose - metabolism
Cytoskeletal Proteins - genetics
Cytoskeletal Proteins - metabolism
death
electron transfer
epigenetics
Humans
Membrane Glycoproteins - genetics
Membrane Glycoproteins - metabolism
metabolism
Mitochondria - genetics
Mitochondria - metabolism
Mitochondrial function
NAD
NAD (coenzyme)
NAD - metabolism
NADP - analogs & derivatives
NADP - metabolism
Oxidation-Reduction
PARP
Poly(ADP-ribose) Polymerases - genetics
Poly(ADP-ribose) Polymerases - metabolism
Protein Processing, Post-Translational
Signal Transduction
SIRTUINS
Sirtuins - genetics
Sirtuins - metabolism
Title NAD and the aging process: Role in life, death and everything in between
URI https://dx.doi.org/10.1016/j.mce.2016.11.003
https://www.ncbi.nlm.nih.gov/pubmed/27825999
https://www.proquest.com/docview/1839124263
https://www.proquest.com/docview/2000301915
https://pubmed.ncbi.nlm.nih.gov/PMC5419884
Volume 455
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