Evidence map›Paper›PMID 23742622›Full record

ReviewCritical reviews in biochemistry and molecular biology

NAD⁺ metabolism: a therapeutic target for age-related metabolic disease.

Laurent Mouchiroud, Riekelt H Houtkooper, Johan Auwerx

Abstract readReview
In one paragraph

Review in Critical reviews in biochemistry and molecular biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 2% 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

118 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. In vivo NAD assay reveals the intracellular NAD contents and redox state in healthy human brain and their age dependences.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Trial
  6. Article
  7. Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026
    Review
  8. Metabolic Plasticity in Embryogenesis Throughout the Lens of NADMethods in molecular biology (Clifton, N.J.) · 2026
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Cardiac NADNature cardiovascular research · 2024
    Article
  17. Review
  18. The role of nicotinamide adenine dinucleotide salvage enzymes in cardioprotection.Kardiochirurgia i torakochirurgia polska = Polish journal of cardio-thoracic surgery · 2024
    Review
  19. NADInternational journal of molecular sciences · 2024
    Article
  20. Article

58 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 2 countries.

Laurent Mouchiroud *Laboratory for Integrative and Systems Physiology, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
Riekelt H Houtkooper *Laboratory Genetic Metabolic Diseases, Academic Medical Center, Amsterdam, The Netherlands.
Johan AuwerxLaboratory for Integrative and Systems Physiology, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
École Polytechnique Fédérale de Lausanne · CHAcademic Medical Center · NL

Funding

Skeletal Muscle Basis for Improved Exercise Endurance in RGS14 KOR01HL106511 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 2011 to 2019
$3.8M
European Research Council 231138NHLBI NIH HHS 1R01HL 106511-01A1NHLBI NIH HHS R01 HL106511
6 · The paper itself

Abstract

Nicotinamide adenine dinucleotide (NAD) is a central metabolic cofactor by virtue of its redox capacity, and as such regulates a wealth of metabolic transformations. However, the identification of the longevity protein silent regulator 2 (Sir2), the founding member of the sirtuin protein family, as being NAD⁺-dependent reignited interest in this metabolite. The sirtuins (SIRT1-7 in mammals) utilize NAD⁺ to deacetylate proteins in different subcellular compartments with a variety of functions, but with a strong convergence on optimizing mitochondrial function. Since cellular NAD⁺ levels are limiting for sirtuin activity, boosting its levels is a powerful means to activate sirtuins as a potential therapy for mitochondrial, often age-related, diseases. Indeed, supplying excess precursors, or blocking its utilization by poly(ADP-ribose) polymerase (PARP) enzymes or CD38/CD157, boosts NAD⁺ levels, activates sirtuins and promotes healthy aging. Here, we discuss the current state of knowledge of NAD⁺ metabolism, primarily in relation to sirtuin function. We highlight how NAD⁺ levels change in diverse physiological conditions, and how this can be employed as a pharmacological strategy.

Indexed as

AnimalsHumansMetabolic DiseasesNADSirtuinsNADSirtuins

Identifiers

PMID23742622
PMCPMC3858599
OpenAlexW2089838011

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.