ArticleThe Journal of clinical investigation2022
Boosting NAD+ blunts TLR4-induced type I IFN in control and systemic lupus erythematosus monocytes.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 3 registered trials, which are not on this map. Cited by 52 papers.
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.
Studies of the Pathogenesis and Natural History of Systemic Lupus Erythematosus (SLE)
Collection and Distribution of Blood Components From Healthy Donors for In Vitro Research Use
Study to Evaluate the Effect of Nicotinamide Riboside on Immunity
Who cites it
52 citing papers in PubMed, 61 citations in OpenAlex.
- NAD+ augmentation by nicotinamide riboside engages SLIT2/ROBO1 signaling to attenuate Th17 inflammation in psoriasis.JCI insight · 2026Trial
- Nicotinamide Riboside Supplementation Benefits in Patients With Werner Syndrome: A Double-Blind Randomized Crossover Placebo-Controlled Trial.Aging cell · 2025Trial
- Parabens exposure in systemic lupus erythematosus: insights from network toxicology and molecular docking.BMC pharmacology & toxicology · 2026Article
- SIRT5-dependent regulation of ASL controls arginine metabolism and T cell function.bioRxiv : the preprint server for biology · 2026Article
- Observational
- Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration.Aging cell · 2026 · on this mapArticle
- Redox therapy for neuropsychiatric disorders: Molecular mechanisms and biomarker development.Science advances · 2026Review
- Cytoplasmic NAD/H synthesis via NRK1 regulates inflammatory capacity and promotes survival of CD4Nature communications · 2026Article
- ISG15 orchestrates dynamic crosstalk between mitochondrial fat oxidation and type 1 interferon in myeloid cells.bioRxiv : the preprint server for biology · 2026Article
- Temporal multi-tissue profiling reveals metabolites linked to immune response and malaria parasitemia control.iScience · 2026Article
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- NADJournal of neuroinflammation · 2025Article
- Mitochondrial dysfunction in myeloid cells: a central deficit in autoimmune diseases.Trends in immunology · 2025Review
- NADNature metabolism · 2025Review
- Immunometabolism in systemic lupus erythematosus.Nature reviews. Rheumatology · 2025Review
- Multiomics analysis unveils an inosine-sensitive DNA damage response in neurogenic bladder after spinal cord injury.JCI insight · 2025Article
- RAB4A DRIVES PROINFLAMMATORY CD4Research square · 2025Article
- Metabolic profiles of cutaneous lupus have abnormalities in the nicotinamide adenine dinucleotide pathway.Lupus science & medicine · 2025Article
- Mitochondrial fatty acid oxidation regulates monocytic type I interferon signaling via histone acetylation.Science advances · 2025Article
- 3-MA attenuates collagen-induced arthritis in vivo via anti-inflammatory effect and autophagy inhibition.BMC musculoskeletal disorders · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
BACKGROUNDFasting and NAD+-boosting compounds, including NAD+ precursor nicotinamide riboside (NR), confer antiinflammatory effects. However, the underlying mechanisms and therapeutic potential are incompletely defined.METHODSWe explored the underlying biology in myeloid cells from healthy volunteers following in vivo placebo or NR administration and subsequently tested the findings in vitro in monocytes extracted from patients with systemic lupus erythematosus (SLE).RESULTSRNA-Seq of unstimulated and LPS-activated monocytes implicated NR in the regulation of autophagy and type I IFN signaling. In primary monocytes, NR blunted LPS-induced IFN-β production, and genetic or pharmacological disruption of autophagy phenocopied this effect. Given that NAD+ is a coenzyme in oxidoreductive reactions, metabolomics was performed and identified that NR increased the inosine level. Inosine supplementation similarly blunted autophagy and IFN-β release. Finally, because SLE exhibits type I IFN dysregulation, we assessed the NR effect on monocytes from patients with SLE and found that NR reduced autophagy and IFN-β release.CONCLUSIONWe conclude that NR, in an NAD+-dependent manner and in part via inosine signaling, mediated suppression of autophagy and attenuated type I IFN in myeloid cells, and we identified NR as a potential adjunct for SLE management.TRIAL REGISTRATIONClinicalTrials.gov registration numbers NCT02812238, NCT00001846, and NCT00001372.FUNDINGThis work was supported by the NHLBI and NIAMS Intramural Research divisions.
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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.