ArticleeLife2024
Functional identification of soluble uric acid as an endogenous inhibitor of CD38.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- The Gut Microbiota-Metabolite-Host Axis in Cardiometabolic Diseases: Bridging Bench to Bedside.Cardiovascular drugs and therapy · 2026Review
- The GPX3-VCAM1 Axis Gates Pro-Fibrotic Tubule Cell Fate in Hyperuricemic Nephropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Uric Acid as a Redox Switch in Gout: Linking Xanthine Oxidoreductase-Derived ROS, NLRP3 Inflammasome Activation and Emerging Ferroptotic Mechanisms.Antioxidants (Basel, Switzerland) · 2026Review
- Emerging chemical strategies for CD38 inhibition: restoring NADBioorganic & medicinal chemistry · 2026Review
- From soluble uric acid to sodium urate crystal: immune metabolic inflammation driven by uric acid morphological transformation and mechanism-oriented therapy.Frontiers in immunology · 2026Review
- Pathological Mechanisms in Sjögren's Disease Likely Involve the ADP-Ribosyl Cyclase Family Members: CD38 and CD157.International journal of molecular sciences · 2025Article
- The Dual Role of Uric Acid: Pathological Implications Across Chronic Diseases and Current Approaches to Hyperuricemia Management.Discoveries (Craiova, Romania)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Excessive elevation or reduction of soluble uric acid (sUA) levels has been linked to some of pathological states, raising another subject that sUA at physiological levels may be essential for the maintenance of health. Yet, the fundamental physiological functions and molecular targets of sUA remain largely unknown. Using enzyme assays and in vitro and in vivo metabolic assays, we demonstrate that sUA directly inhibits the hydrolase and cyclase activities of CD38 via a reversible non-competitive mechanism, thereby limiting nicotinamide adenine dinucleotide (NAD
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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.