ArticleThe Journal of biological chemistry2013
Regulation of the Na+/Ca2+ exchanger by pyridine nucleotide redox potential in ventricular myocytes.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Understanding molecular mechanisms driving cadmium-induced mitochondrial dysfunction in human metabolic liver disease.Environmental toxicology and pharmacology · 2026Review
- Role of NaInternational journal of molecular sciences · 2023Article
- NALCN-mediated sodium influx confers metastatic prostate cancer cell invasiveness.The EMBO journal · 2023Article
- Review
- Preventing unfolded protein response-induced ion channel dysregulation to treat arrhythmias.Trends in molecular medicine · 2022Review
- PDE1 Inhibition Modulates CaCirculation research · 2021Article
- Metabolic regulation of Kv channels and cardiac repolarization by Kvβ2 subunits.Journal of molecular and cellular cardiology · 2019Article
- Hypertrophic Cardiomyopathy: A Vicious Cycle Triggered by Sarcomere Mutations and Secondary Disease Hits.Antioxidants & redox signaling · 2019Review
- Altered Intracellular Calcium Homeostasis and Arrhythmogenesis in the Aged Heart.International journal of molecular sciences · 2019Review
- Protective effects of gallic acid on cardiac electrophysiology and arrhythmias during reperfusion in diabetes.Iranian journal of basic medical sciences · 2019Article
- Regional increase in ROS within stretched region exacerbates arrhythmias in rat trabeculae with nonuniform contraction.Pflugers Archiv : European journal of physiology · 2018Article
- Emerging potential benefits of modulating NADAmerican journal of physiology. Heart and circulatory physiology · 2018Review
- Allele-specific differences in transcriptome, miRNome, and mitochondrial function in two hypertrophic cardiomyopathy mouse models.JCI insight · 2018Article
- Proarrhythmic Remodeling of Calcium Homeostasis in Cardiac Disease; Implications for Diabetes and Obesity.Frontiers in physiology · 2018Review
- Pyruvate enhancement of cardiac performance: Cellular mechanisms and clinical application.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- The Role of Sodium in Diabetic Cardiomyopathy.Frontiers in physiology · 2018Review
- Kvβ1.1 (AKR6A8) senses pyridine nucleotide changes in the mouse heart and modulates cardiac electrical activity.American journal of physiology. Heart and circulatory physiology · 2017Article
- How cardiomyocytes sense pathophysiological stresses for cardiac remodeling.Cellular and molecular life sciences : CMLS · 2017Review
- Regulation of signal transduction by reactive oxygen species in the cardiovascular system.Circulation research · 2015Review
- Hypertrophic cardiomyopathy: a heart in need of an energy bar?Frontiers in physiology · 2014Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The cardiac Na(+)/Ca(2+) exchanger (NCX) is the major Ca(2+) efflux pathway on the sarcolemma, counterbalancing Ca(2+) influx via L-type Ca(2+) current during excitation-contraction coupling. Altered NCX activity modulates the sarcoplastic reticulum Ca(2+) load and can contribute to abnormal Ca(2+) handling and arrhythmias. NADH/NAD(+) is the main redox couple controlling mitochondrial energy production, glycolysis, and other redox reactions. Here, we tested whether cytosolic NADH/NAD(+) redox potential regulates NCX activity in adult cardiomyocytes. NCX current (INCX), measured with whole cell patch clamp, was inhibited in response to cytosolic NADH loaded directly via pipette or increased by extracellular lactate perfusion, whereas an increase of mitochondrial NADH had no effect. Reactive oxygen species (ROS) accumulation was enhanced by increasing cytosolic NADH, and NADH-induced INCX inhibition was abolished by the H2O2 scavenger catalase. NADH-induced ROS accumulation was independent of mitochondrial respiration (rotenone-insensitive) but was inhibited by the flavoenzyme blocker diphenylene iodonium. NADPH oxidase was ruled out as the effector because INCX was insensitive to cytosolic NADPH, and NADH-induced ROS and INCX inhibition were not abrogated by the specific NADPH oxidase inhibitor gp91ds-tat. This study reveals a novel mechanism of NCX regulation by cytosolic NADH/NAD(+) redox potential through a ROS-generating NADH-driven flavoprotein oxidase. The mechanism is likely to play a key role in Ca(2+) homeostasis and the response to alterations in the cytosolic pyridine nucleotide redox state during ischemia-reperfusion or other cardiovascular diseases.
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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.