ArticleJCI insight2017
Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich's ataxia cardiomyopathy model.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
What it found
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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.
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Who cites it
88 citing papers in PubMed, 128 citations in OpenAlex.
- Safety and efficacy of individualised exercise and NADThe Lancet. Neurology · 2026Trial
- Nicotinamide mononucleotide supplementation enhances aerobic capacity in amateur runners: a randomized, double-blind study.Journal of the International Society of Sports Nutrition · 2021Trial
- NAMPT activation uncovers a senescence-specific vulnerability and promotes healthy aging in combination with NAM.bioRxiv : the preprint server for biology · 2026Article
- Gravitational and mechanical forces shape mitochondrial translation.Nature communications · 2026Article
- Nicotinamide riboside prevents mitochondrial dysfunction in nemaline myopathy type 6.Human molecular genetics · 2026Article
- An integrated anti-aging framework targeting NADRedox biology · 2026Review
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- NADMetabolites · 2025Article
- Nicotinamide Adenine Dinucleotide Supplementation to Alleviate Heart Failure: A Mitochondrial Dysfunction Perspective.Nutrients · 2025Review
- Mitochondrial NADNature cardiovascular research · 2025Article
- Nicotinamide Mononucleotide and Nicotinamide Riboside Improve Dyslipidemia and Fatty Liver but Promote Atherosclerosis in Apolipoprotein E Knockout Mice.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Microtubules Sequester Acetylated YAP in the Cytoplasm and Inhibit Heart Regeneration.Circulation · 2025Article
- Pathobiochemistry of Aging and Neurodegeneration: Deregulation of NAD+ Metabolism in Brain Cells.Biomolecules · 2024Review
- NADCell communication and signaling : CCS · 2024Review
- NAD metabolism and heart failure: Mechanisms and therapeutic potentials.Journal of molecular and cellular cardiology · 2024Review
- Nicotinamide Mononucleotide: Research Process in Cardiovascular Diseases.International journal of molecular sciences · 2024Review
- Advancements in NMN biotherapy and research updates in the field of digestive system diseases.Journal of translational medicine · 2024Review
- Advances in the Synthesis and Physiological Metabolic Regulation of Nicotinamide Mononucleotide.Nutrients · 2024Review
- NAD+ precursors prolong survival and improve cardiac phenotypes in a mouse model of Friedreich's Ataxia.JCI insight · 2024Article
- Nicotinamide Mononucleotide Supplementation: Understanding Metabolic Variability and Clinical Implications.Metabolites · 2024Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Increasing NAD+ levels by supplementing with the precursor nicotinamide mononucleotide (NMN) improves cardiac function in multiple mouse models of disease. While NMN influences several aspects of mitochondrial metabolism, the molecular mechanisms by which increased NAD+ enhances cardiac function are poorly understood. A putative mechanism of NAD+ therapeutic action exists via activation of the mitochondrial NAD+-dependent protein deacetylase sirtuin 3 (SIRT3). We assessed the therapeutic efficacy of NMN and the role of SIRT3 in the Friedreich's ataxia cardiomyopathy mouse model (FXN-KO). At baseline, the FXN-KO heart has mitochondrial protein hyperacetylation, reduced Sirt3 mRNA expression, and evidence of increased NAD+ salvage. Remarkably, NMN administered to FXN-KO mice restores cardiac function to near-normal levels. To determine whether SIRT3 is required for NMN therapeutic efficacy, we generated SIRT3-KO and SIRT3-KO/FXN-KO (double KO [dKO]) models. The improvement in cardiac function upon NMN treatment in the FXN-KO is lost in the dKO model, demonstrating that the effects of NMN are dependent upon cardiac SIRT3. Coupled with cardio-protection, SIRT3 mediates NMN-induced improvements in both cardiac and extracardiac metabolic function and energy metabolism. Taken together, these results serve as important preclinical data for NMN supplementation or SIRT3 activator therapy in Friedreich's ataxia patients.
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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.