ReviewCells2022
Nicotinamide Adenine Dinucleotide (NAD) Metabolism as a Relevant Target in Cancer.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Sensitizing Colorectal Cancer to PARP Inhibitors: Biomarkers, Mechanisms, and Combination Strategies.International journal of molecular sciences · 2026Review
- Computational Identification of New Dual PAK4 and NAMPT Inhibitors.International journal of molecular sciences · 2026Article
- Metabolic Engineering ofMicroorganisms · 2026Article
- Nanomedicine-powered redox homeostasis modulation: Disrupting antioxidant systems and inducing oxidative stress for precision tumor therapy.Materials today. Bio · 2026Review
- Promotion of breast cancer by the DNPH1 enzyme.iScience · 2026Article
- The role of NADFrontiers in oncology · 2026Review
- Integration of tumor microenvironment and metabolic signatures reveals TMPI-defined prognostic and immunotherapy-relevant phenotypes in breast cancer.Frontiers in pharmacology · 2026Article
- PPA1 promotes oxidative phosphorylation and malignant progression of colorectal cancer under glucose restriction via AMPK/ULK1/FUNDC1-mediated mitophagy.Cell death discovery · 2025Article
- Glutaminase inhibitor CB-839 causes metabolic adjustments in colorectal cancer cells.Scientific reports · 2025Article
- Temozolomide-Derived AIC Is Incorporated into Purine Synthesis in Glioblastoma.Chemical research in toxicology · 2025Article
- Deciphering enemy tactics - the narrow path to an optimal anti-cancer strategy targeting the Warburg effect.Pharmacological reports : PR · 2025Review
- Crosstalk Between Metabolic Reprogramming and Epigenetic Modifications in Colorectal Cancer: Mechanisms and Clinical Applications.Current issues in molecular biology · 2025Review
- Efficacy of NAMPT Inhibitors in Pancreatic Cancer After Stratification by MAP17 (PDZK1IP1) Levels.Cancers · 2025Article
- Targeted protein degradation with small molecules for cancer immunotherapy.Asian journal of pharmaceutical sciences · 2025Review
- Application of Metabolic Biomarkers in Breast Cancer: A Literature Review.Annals of laboratory medicine · 2025Review
- Unveiling the future of cancer stem cell therapy: a narrative exploration of emerging innovations.Discover oncology · 2025Review
- Targeting NAD + biosynthesis suppresses TGF-β1/Smads/RAB26 axis and potentiates cisplatin cytotoxicity in non-small cell lung cancer brain metastasis.Acta neuropathologica communications · 2025Article
- Value of serum tryptophan in stratified management of 90-day mortality risk in patients with hepatitis B virus-related acute-on-chronic liver failure: a multicenter retrospective study.Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- NADH supplementation improves human oocyte maturation and developmental competence of resulting embryos in controlled ovarian hyperstimulation cycles: a pilot study implicating the CDK2/GAS6 signaling pathway.Frontiers in endocrinology · 2025Article
- Macrophages in osteoporotic fractures: from immunometabolic mechanisms to precision therapeutic approaches.Frontiers in endocrinology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NAD+ is an important metabolite in cell homeostasis that acts as an essential cofactor in oxidation-reduction (redox) reactions in various energy production processes, such as the Krebs cycle, fatty acid oxidation, glycolysis and serine biosynthesis. Furthermore, high NAD+ levels are required since they also participate in many other nonredox molecular processes, such as DNA repair, posttranslational modifications, cell signalling, senescence, inflammatory responses and apoptosis. In these nonredox reactions, NAD+ is an ADP-ribose donor for enzymes such as sirtuins (SIRTs), poly-(ADP-ribose) polymerases (PARPs) and cyclic ADP-ribose (cADPRs). Therefore, to meet both redox and nonredox NAD+ demands, tumour cells must maintain high NAD+ levels, enhancing their synthesis mainly through the salvage pathway. NAMPT, the rate-limiting enzyme of this pathway, has been identified as an oncogene in some cancer types. Thus, NAMPT has been proposed as a suitable target for cancer therapy. NAMPT inhibition causes the depletion of NAD+ content in the cell, leading to the inhibition of ATP synthesis. This effect can cause a decrease in tumour cell proliferation and cell death, mainly by apoptosis. Therefore, in recent years, many specific inhibitors of NAMPT have been developed, and some of them are currently in clinical trials. Here we review the NAD metabolism as a cancer therapy target.
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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.