ArticleHeart rhythm2017
Role of protein kinase C in metabolic regulation of the cardiac Na
Article in Heart rhythm, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Cardiac TRPM7 Causes Diabetic Heart Failure With Preserved Ejection Fraction.JACC. Basic to translational science · 2025Article
- Voltage-Gated Sodium Channels: A Therapeutic Target in Ischemic Heart Disease.Reviews in cardiovascular medicine · 2025Review
- Modulation of NOX2 causes obesity-mediated atrial fibrillation.The Journal of clinical investigation · 2024Article
- Protein Kinase C (PKC) in Neurological Health: Implications for Alzheimer's Disease and Chronic Alcohol Consumption.Brain sciences · 2024Review
- Role of Protein Kinase C in Metabolic Regulation of Coronary Endothelial Small Conductance Calcium-Activated Potassium Channels.Journal of the American Heart Association · 2024Article
- GPD1L-A306del modifies sodium current in a family carrying the dysfunctional SCN5A-G1661R mutation associated with Brugada syndrome.Pflugers Archiv : European journal of physiology · 2024Article
- Acute protein kinase C beta inhibition preserves coronary endothelial function after cardioplegic hypoxia/reoxygenation.JTCVS open · 2023Article
- TRPM7 kinase mediates hypomagnesemia-induced seizure-related death.Scientific reports · 2023Article
- Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance.Cardiovascular research · 2023Review
- Metabolic rescue ameliorates mitochondrial encephalo-cardiomyopathy in murine and human iPSC models of Leigh syndrome.Clinical and translational medicine · 2022Article
- Preventing unfolded protein response-induced ion channel dysregulation to treat arrhythmias.Trends in molecular medicine · 2022Review
- Genomic and Non-Genomic Regulatory Mechanisms of the Cardiac Sodium Channel in Cardiac Arrhythmias.International journal of molecular sciences · 2022Review
- Inhibition of the unfolded protein response reduces arrhythmia risk after myocardial infarction.The Journal of clinical investigation · 2021Article
- Magnesium Deficiency Causes a Reversible, Metabolic, Diastolic Cardiomyopathy.Journal of the American Heart Association · 2021Article
- Mitochondrial Dysfunction Increases Arrhythmic Triggers and Substrates; Potential Anti-arrhythmic Pharmacological Targets.Frontiers in cardiovascular medicine · 2021Review
- Ethanol Disrupts Hormone-Induced Calcium Signaling in Liver.Function (Oxford, England) · 2021Article
- The endosomal trafficking regulator LITAF controls the cardiac Nav1.5 channel via the ubiquitin ligase NEDD4-2.The Journal of biological chemistry · 2020Article
- MIR448 antagomir reduces arrhythmic risk after myocardial infarction by upregulating the cardiac sodium channel.JCI insight · 2020Article
- Magnesium, Oxidative Stress, Inflammation, and Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Ion Channel and Structural Remodeling in Obesity-Mediated Atrial Fibrillation.Circulation. Arrhythmia and electrophysiology · 2020Article
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 4 institutions in 2 countries.
Funding
Abstract
backgroundThe reduced form of nicotinamide adenine dinucleotide (NADH) increases in cardiomyopathy, activates protein kinase C (PKC), up-regulates mitochondrial reactive oxygen species (mitoROS), and down-regulates the cardiac Na
objectiveThe purpose of this study was to determine how NADH signals down-regulation of Na
methodsIsolated mouse cardiomyocytes were used for patch-clamp recording and for monitoring mitoROS with MitoSOX Red. HEK293 cells were used for transient transfections. HEK293 cells stably expressing human Na
resultsNADH enhanced PLD activity (1.6- ± 0.1-fold, P <.01) and activated PKCδ. Activated PKCδ translocated to mitochondria and up-regulated mitoROS (2.8- ± 0.3-fold, P <.01) by enhancing the activities of mitochondrial complexes I, II, and IV (1.1- to 1.5-fold, P <.01). PKCδ also interacted with Na
conclusionNADH activated PKCδ by enhancing PLD activity. PKCδ modulated both mitoROS and Na
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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.