Evidence map›Paper›PMID 27825999›Full record

ReviewMolecular and cellular endocrinology2017

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

Claudia C S Chini, Mariana G Tarragó, Eduardo N Chini

Abstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
11.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

137 citing papers in PubMed, 201 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Metabolic Brain Disorders: Prodromes, Symptoms, and Syndromes.International journal of molecular sciences · 2026
    Review
  6. Article
  7. NADAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Biomolecular Basis of Life.Metabolites · 2025
    Review
  18. Review
  19. Review
  20. Protein Acetylation and NAD+ Homeostasis in Aging Muscle.Advances in experimental medicine and biology · 2025
    Review

77 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Claudia C S ChiniSignal Transduction Laboratory, Kogod Aging Center, Department of Anesthesiology, Oncology Research, GI Signaling Center, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Mariana G TarragóSignal Transduction Laboratory, Kogod Aging Center, Department of Anesthesiology, Oncology Research, GI Signaling Center, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Eduardo N ChiniSignal Transduction Laboratory, Kogod Aging Center, Department of Anesthesiology, Oncology Research, GI Signaling Center, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. Electronic address: chini.eduardo@mayo.edu.
WinnMed · USMayo Clinic · US

Funding

Tissue CoreP50CA102701 · NCI · MAYO CLINIC ROCHESTER · PI PETERSEN, GLORIA M. · 2004 to 2018
$32.7M
The Sir2-p53-IGF Link in Mammalian Life-Span ControlR01AG026094 · NIA · UNIVERSITY OF VIRGINIA · PI CHINI, EDUARDO N · 2006 to 2016
$3.8M
NCI NIH HHS P50 CA102701NIA NIH HHS R01 AG026094
6 · The paper itself

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.

Indexed as

Caloric RestrictionProtein Processing, Post-TranslationalADP-ribosyl Cyclase 1AgingAnimalsArmadillo Domain ProteinsCyclic ADP-RiboseCytoskeletal ProteinsHumansMembrane GlycoproteinsMitochondriaNADNADPOxidation-ReductionPoly(ADP-ribose) PolymerasesSignal TransductionADP-ribosyl Cyclase 1Armadillo Domain ProteinsCD38 protein, humanCyclic ADP-RiboseCytoskeletal ProteinsMembrane GlycoproteinsNAADPNADNADPPoly(ADP-ribose) PolymerasesSARM1 protein, humanSirtuinsAgingCD38Mitochondrial functionNAD(+)PARPSIRTUINS

Identifiers

PMID27825999
PMCPMC5419884
OpenAlexW2548864808

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.