ArticleJournal of the American Heart Association2024
Role of Protein Kinase C in Metabolic Regulation of Coronary Endothelial Small Conductance Calcium-Activated Potassium Channels.
Article in Journal of the American Heart Association, 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 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
7 citing papers in PubMed.
- Bilobalide increases SKBMC complementary medicine and therapies · 2026Article
- The Emerging Role of Endothelial Ion Channels in the Control of Human Microcirculation.International journal of molecular sciences · 2026Review
- Cross-phenotype integration of eQTL-based Mendelian randomization and transcriptomics prioritizesFrontiers in immunology · 2026Article
- Effects of metabolic syndrome and its components on myocardial microcirculation in obstructive coronary artery disease patients: a CMR perfusion study.Cardiovascular diabetology · 2025Article
- Protein Kinase C-β Inhibition and Survival Signaling after Simulated Cardioplegic-Ischemia/Reperfusion in Nondiabetic and Diabetic Human Coronary Arterial Endothelial Cells.Journal of the American College of Surgeons · 2025Article
- Potential Effect of Cinnamaldehyde on Insulin Resistance Is Mediated by Glucose and Lipid Homeostasis.Nutrients · 2025Article
- Linking oxidative stress biomarkers to disease progression and antioxidant therapy in hypertension and diabetes mellitus.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundSmall conductance calcium-activated potassium (SK) channels are largely responsible for endothelium-dependent coronary arteriolar relaxation. Endothelial SK channels are downregulated by the reduced form of nicotinamide adenine dinucleotide (NADH), which is increased in the setting of diabetes, yet the mechanisms of these changes are unclear. PKC (protein kinase C) is an important mediator of diabetes-induced coronary endothelial dysfunction. Thus, we aimed to determine whether NADH signaling downregulates endothelial SK channel function via PKC. METHODS AND
resultsSK channel currents of human coronary artery endothelial cells were measured by whole cell patch clamp method in the presence/absence of NADH, PKC activator phorbol 12-myristate 13-acetate, PKC inhibitors, or endothelial PKC
conclusionsNADH-induced inhibition of endothelial SK channel function is mediated via PKC
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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 Socratic graph.