ArticleThe Journal of pharmacology and experimental therapeutics2017
Luteolinidin Protects the Postischemic Heart through CD38 Inhibition with Preservation of NAD(P)(H).
Article in The Journal of pharmacology and experimental therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- The Search for Drugs Derived from Natural Products forCurrent topics in medicinal chemistry · 2024Pooled it
- Large-Scale Plasma Proteomics and Genetic Integration Uncover Novel Biological Pathways in Male Pattern Baldness.International journal of molecular sciences · 2026Article
- NAD + in fatty liver disease: mechanistic insights and associated targets.Cell biology and toxicology · 2025Review
- Potential dietary geroprotectors and their impact on key mechanisms of aging.Biogerontology · 2025Review
- CD38 connects the heart and brain.Translational psychiatry · 2025Review
- Nicotinamide Adenine Dinucleotide Supplementation to Alleviate Heart Failure: A Mitochondrial Dysfunction Perspective.Nutrients · 2025Review
- NADCell communication and signaling : CCS · 2024Review
- Inhibition of CD38 enzymatic activity enhances CAR-T cell immune-therapeutic efficacy by repressing glycolytic metabolism.Cell reports. Medicine · 2024Article
- The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review.Journal of thoracic disease · 2023Review
- Effects of Apocynin, a NADPH Oxidase Inhibitor, in the Protection of the Heart from Ischemia/Reperfusion Injury.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Review
- Potential Synergistic Supplementation of NAD+ Promoting Compounds as a Strategy for Increasing Healthspan.Nutrients · 2023Review
- Premature senescence and cardiovascular disease following cancer treatments: mechanistic insights.Frontiers in cardiovascular medicine · 2023Review
- Research Progress on Absorption, Metabolism, and Biological Activities of Anthocyanins in Berries: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Targeting CD38 in Neoplasms and Non-Cancer Diseases.Cancers · 2022Review
- Reduced nicotinamide adenine dinucleotide phosphate in redox balance and diseases: a friend or foe?Acta pharmacologica Sinica · 2022Review
- NADJournal of lipid and atherosclerosis · 2022Review
- Cancer treatment-induced NAD+ depletion in premature senescence and late cardiovascular complications.The journal of cardiovascular aging · 2022Article
- Characterizing CD38 Expression and Enzymatic Activity in the Brain of Spontaneously Hypertensive Stroke-Prone Rats.Frontiers in pharmacology · 2022Article
- CD38: A Potential Therapeutic Target in Cardiovascular Disease.Cardiovascular drugs and therapy · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
We recently showed that ischemia/reperfusion (I/R) of the heart causes CD38 activation with resultant depletion of the cardiac NADP(H) pool, which is most marked in the endothelium. This NADP(H) depletion was shown to limit the production of nitric oxide by endothelial nitric oxide synthase (eNOS), which requires NADPH for nitric oxide production, resulting in greatly altered endothelial function. Therefore, intervention with CD38 inhibitors could reverse postischemic eNOS-mediated endothelial dysfunction. Here, we evaluated the potency of the CD38 inhibitor luteolinidin, an anthocyanidin, at blocking CD38 activity and preserving endothelial and myocardial function in the postischemic heart. Initially, we characterized luteolinidin as a CD38 inhibitor in vitro to determine its potency and mechanism of inhibition. We then tested luteolinidin in the ex vivo isolated heart model, where we determined luteolinidin uptake with aqueous and liposomal delivery methods. Optimal delivery methods were then further tested to determine the effect of luteolinidin on postischemic NAD(P)(H) and tetrahydrobiopterin levels. Finally, through nitric oxide synthase-dependent coronary flow and left ventricular functional measurements, we evaluated the efficacy of luteolinidin to protect vascular and contractile function, respectively, after I/R. With enhanced postischemic preservation of NADPH and tetrahydrobiopterin, there was a dose-dependent effect of luteolinidin on increasing recovery of endothelium-dependent vasodilatory function, as well as enhancing the recovery of left ventricular contractile function with increased myocardial salvage. Thus, luteolinidin is a potent CD38 inhibitor that protects the heart against I/R injury with preservation of eNOS function and prevention of endothelial dysfunction.
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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.