ArticleJournal of cardiovascular pharmacology and therapeutics2016
Nicorandil, a Nitric Oxide Donor and ATP-Sensitive Potassium Channel Opener, Protects Against Dystrophin-Deficient Cardiomyopathy.
Article in Journal of cardiovascular pharmacology and therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 50 citations in OpenAlex.
- Dystrophin Loss in Engineered Heart Tissues Recapitulates Clinically Relevant Aspects of Dystrophic Cardiomyopathy.Journal of biomechanical engineering · 2026Article
- High mobility group box 1 (HMGB1) is a potential disease biomarker in cell and mouse models of Duchenne muscular dystrophy.Biology open · 2024Article
- Therapeutic potential of nicorandil beyond anti-anginal drug: A review on current and future perspectives.Heliyon · 2024Review
- Review
- Sleeve Gastrectomy Provides Cardioprotection from Oxidative Stress In Vitro Due to Reduction of Circulating Myeloperoxidase.Nutrients · 2023Article
- Induced Pluripotent Stem Cells for Tissue-Engineered Skeletal Muscles.International journal of molecular sciences · 2023Review
- Modeling Duchenne Muscular Dystrophy Cardiomyopathy with Patients' Induced Pluripotent Stem-Cell-Derived Cardiomyocytes.International journal of molecular sciences · 2023Review
- ACTA1 H40Y mutant iPSC-derived skeletal myocytes display mitochondrial defects in an in vitro model of nemaline myopathy.Experimental cell research · 2023Article
- Induced Pluripotent Stem Cells for Modeling Physiological and Pathological Striated Muscle Complexity.Journal of neuromuscular diseases · 2023Review
- Protective effect of ischaemic postconditioning combined with nicorandil on myocardial ischaemia‒reperfusion injury in diabetic rats.BMC cardiovascular disorders · 2022Article
- Adverse event profiles of microscopic colitis in the Japanese Adverse Drug Event Report (JADER) database.Scientific reports · 2022Article
- Alternative Targets for Modulators of Mitochondrial Potassium Channels.Molecules (Basel, Switzerland) · 2022Review
- Combined Systemic Intake of K-ATP Opener (Nicorandil) and Mesenchymal Stem Cells Preconditioned With Nicorandil Alleviates Pancreatic Insufficiency in a Model of Bilateral Renal Ischemia/Reperfusion Injury.Frontiers in physiology · 2022Article
- Cardiomyocyte-produced miR-339-5p mediates pathology in Duchenne muscular dystrophy cardiomyopathy.Human molecular genetics · 2021Article
- Perspectives on hiPSC-Derived Muscle Cells as Drug Discovery Models for Muscular Dystrophies.International journal of molecular sciences · 2021Review
- Nicorandil decreases oxidative stress in slow- and fast-twitch muscle fibers of diabetic rats by improving the glutathione system functioning.Journal of diabetes investigation · 2021Article
- Cardioprotective effect of nicorandil on isoproterenol induced cardiomyopathy in the Mdx mouse model.BMC cardiovascular disorders · 2021Article
- Influence of microRNAs and exosomes in muscle health and diseases.Journal of muscle research and cell motility · 2020Article
- Duchenne muscular dystrophy (DMD) cardiomyocyte-secreted exosomes promote the pathogenesis of DMD-associated cardiomyopathy.Disease models & mechanisms · 2020Article
- "Betwixt Mine Eye and Heart a League Is Took": The Progress of Induced Pluripotent Stem-Cell-Based Models of Dystrophin-Associated Cardiomyopathy.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDystrophin-deficient cardiomyopathy is a growing clinical problem without targeted treatments. We investigated whether nicorandil promotes cardioprotection in human dystrophin-deficient induced pluripotent stem cell (iPSC)-derived cardiomyocytes and the muscular dystrophy mdx mouse heart. METHODS AND
resultsDystrophin-deficient iPSC-derived cardiomyocytes had decreased levels of endothelial nitric oxide synthase and neuronal nitric oxide synthase. The dystrophin-deficient cardiomyocytes had increased cell injury and death after 2 hours of stress and recovery. This was associated with increased levels of reactive oxygen species and dissipation of the mitochondrial membrane potential. Nicorandil pretreatment was able to abolish these stress-induced changes through a mechanism that involved the nitric oxide-cyclic guanosine monophosphate pathway and mitochondrial adenosine triphosphate-sensitive potassium channels. The increased reactive oxygen species levels in the dystrophin-deficient cardiomyocytes were associated with diminished expression of select antioxidant genes and increased activity of xanthine oxidase. Furthermore, nicorandil was found to improve the restoration of cardiac function after ischemia and reperfusion in the isolated mdx mouse heart.
conclusionNicorandil protects against stress-induced cell death in dystrophin-deficient cardiomyocytes and preserves cardiac function in the mdx mouse heart subjected to ischemia and reperfusion injury. This suggests a potential therapeutic role for nicorandil in dystrophin-deficient cardiomyopathy.
Indexed as
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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.