ArticleJournal of cellular and molecular medicine2019
Nicotinamide reduces renal interstitial fibrosis by suppressing tubular injury and inflammation.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 90 citations in OpenAlex.
- Tubulointerstitial inflammation in glomerular diseases: mechanistic pathways, prognostic value, and translational therapeutic targets.Renal failure · 2026Review
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Protection against cisplatin-induced acute kidney injury by hellgrammite extract: insights from comprehensive metabolomics.Frontiers in pharmacology · 2026Article
- Article
- Nicotinamide Attenuates Complement and Coagulation Pathways and Resultant Renal Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- NADTrends in molecular medicine · 2025Review
- Genetic Factors Related to the Development or Progression of Mesoamerican Endemic Nephropathy.International journal of molecular sciences · 2025Review
- Article
- CircPWWP2A promotes renal interstitial fibrosis through modulating miR-182/ROCK1 axis.Renal failure · 2024Article
- NADCell communication and signaling : CCS · 2024Review
- Article
- Nicotinamide mitigates visceral leishmaniasis by regulating inflammatory response and enhancing lipid metabolism.Parasites & vectors · 2024Article
- Tubular insulin-induced gene 1 deficiency promotes NADEMBO molecular medicine · 2024Article
- Derangement in Nicotinamide Adenine Dinucleotide Metabolism is Observed During Acute Kidney Injury Among Male Agricultural Workers at Risk for Mesoamerican Nephropathy.Kidney international reports · 2024Article
- Therapeutic application of nicotinamide: As a potential target for inhibiting fibrotic scar formation following spinal cord injury.CNS neuroscience & therapeutics · 2024Article
- The role and therapeutic targeting of the CCL2/CCR2 signaling axis in inflammatory and fibrotic diseases.Frontiers in immunology · 2024Review
- α-methyltryptophan-mediated protection against diabetic nephropathy inFrontiers in pharmacology · 2024Article
- Article
- The complexity of nicotinamide adenine dinucleotide (NAD), hypoxic, and aryl hydrocarbon receptor cell signaling in chronic kidney disease.Journal of translational medicine · 2023Review
- Time-of-day defines NADNature communications · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal interstitial fibrosis is a common pathological feature in progressive kidney diseases currently lacking effective treatment. Nicotinamide (NAM), a member of water-soluble vitamin B family, was recently suggested to have a therapeutic potential for acute kidney injury (AKI) in mice and humans. The effect of NAM on chronic kidney pathologies, including renal fibrosis, is unknown. Here we have tested the effects of NAM on renal interstitial fibrosis using in vivo and in vitro models. In vivo, unilateral urethral obstruction (UUO) induced renal interstitial fibrosis as indicated Masson trichrome staining and expression of pro-fibrotic proteins, which was inhibited by NAM. In UUO, NAM suppressed tubular atrophy and apoptosis. In addition, NAM suppressed UUO-associated T cell and macrophage infiltration and induction of pro-inflammatory cytokines, such as TNF-α and IL-1β. In cultured mouse proximal tubule cells, NAM blocked TGF-β-induced expression of fibrotic proteins, while it marginally suppressed the morphological changes induced by TGF-β. NAM also suppressed the expression of pro-inflammatory cytokines (eg MCP-1 and IL-1β) during TGF-β treatment of these cells. Collectively, the results demonstrate an anti-fibrotic effect of NAM in kidneys, which may involve the suppression of tubular injury and inflammation.
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.