ArticleCell2013
The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling.
Article in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 717 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
717 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,204 citations in OpenAlex.
- Effects of Nicotinamide Mononucleotide Supplementation on Blood Pressure: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.Nutrients · 2026Pooled it
- NADFrontiers in neurology · 2026Pooled it
- Sublingual NMN administration increases early circulating terminal catabolites 2PY and 4PY compared with oral administration in healthy adult men.Scientific reports · 2026Trial
- Genetic modulation of NAD(P)H homeostasis reveals distinct redox-coupled metabolic vulnerabilities.Nature metabolism · 2026Article
- Mitochondrial NADP(H)-dependent de novo dTMP biosynthesis counteracts the cytotoxicity of PARP inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Inducible chronic NAD deficiency in mice reveals multi-systemic phenotypical, metabolic, and transcriptional changes.Nature communications · 2026Article
- Metabolic and Immunometabolic Neuroprotection in Glaucoma: Mitochondrial Dysfunction, Neuroinflammation, and Emerging Therapeutic Strategies.Molecules (Basel, Switzerland) · 2026Review
- A multilayered stress-response circuit: The mammalian mitochondrial UPR.The FEBS journal · 2026Review
- A Mechanism-Based Framework for Anti-Aging Strategies: From Metabolic Regulation to Senotherapy and Stem Cell-Based Interventions.Aging cell · 2026Review
- The senescence-stiffening loop: Extracellular matrix remodeling, hypoperfusion, and mitochondrial dysfunction drive tissue aging.Cell metabolism · 2026Review
- Exercise elicits mitonuclear protein imbalance and UPRJournal of physiology and biochemistry · 2026Article
- Aging regulation by gut microbiota: molecular insights from Caenorhabditis elegans.Biogerontology · 2026Review
- Article
- Repetitive Compressive Loading Downregulates the Expression of Autophagy-Related Factors, Autophagy Capacity and Cellular Activity in Human Osteoarthritic Chondrocytes.International journal of molecular sciences · 2026Article
- Positioning TERT at the apex of aging.Nature aging · 2026Review
- Redox Molecules in Aging and Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- [Systemic Reprogramming of Cellular Senescence: Coordinated Regulation of Metabolism, Epigenetics, and Proteostasis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Review
- Article
- Delayed molecular aging, preservation of energy metabolism and enhanced exercise response in exercise-trained human muscle.Nature aging · 2026Article
- Bacteria-derived glutarate mitigates Alzheimer's disease model pathology through autophagy-lysosomal pathway.Cell communication and signaling : CCS · 2026Article
657 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 3 countries.
Funding
Abstract
NAD(+) is an important cofactor regulating metabolic homeostasis and a rate-limiting substrate for sirtuin deacylases. We show that NAD(+) levels are reduced in aged mice and Caenorhabditis elegans and that decreasing NAD(+) levels results in a further reduction in worm lifespan. Conversely, genetic or pharmacological restoration of NAD(+) prevents age-associated metabolic decline and promotes longevity in worms. These effects are dependent upon the protein deacetylase sir-2.1 and involve the induction of mitonuclear protein imbalance as well as activation of stress signaling via the mitochondrial unfolded protein response (UPR(mt)) and the nuclear translocation and activation of FOXO transcription factor DAF-16. Our data suggest that augmenting mitochondrial stress signaling through the modulation of NAD(+) levels may be a target to improve mitochondrial function and prevent or treat age-associated decline.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.