ArticleDrug discovery today. Disease models2007
The role of Na dysregulation in cardiac disease and how it impacts electrophysiology.
Article in Drug discovery today. Disease models, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Time Course of Cardiac Arrhythmia Following High-Volume Exercise in Recreational Cyclists.Journal of the American Heart Association · 2026Article
- Intracellular sodium elevation reprograms cardiac metabolism.Nature communications · 2020Article
- Mechanisms of ventricular arrhythmias: from molecular fluctuations to electrical turbulence.Annual review of physiology · 2015Review
- Intracellular Na+ overload causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes.Journal of molecular and cellular cardiology · 2014Article
- Mitochondrial Ca2+ uniporter and CaMKII in heart.Nature · 2014Article
- Adrenergic signaling regulates mitochondrial Ca2+ uptake through Pyk2-dependent tyrosine phosphorylation of the mitochondrial Ca2+ uniporter.Antioxidants & redox signaling · 2014Article
- Mitochondrial ion channels/transporters as sensors and regulators of cellular redox signaling.Antioxidants & redox signaling · 2014Review
- Inhibiting mitochondrial Na+/Ca2+ exchange prevents sudden death in a Guinea pig model of heart failure.Circulation research · 2014Article
- NCLX: the mitochondrial sodium calcium exchanger.Journal of molecular and cellular cardiology · 2013Article
- Role of mitochondrial dysfunction in cardiac glycoside toxicity.Journal of molecular and cellular cardiology · 2010Article
- Mitochondria in cardiomyocyte Ca2+ signaling.The international journal of biochemistry & cell biology · 2009Review
- Regulation of mitochondrial Ca2+ and its effects on energetics and redox balance in normal and failing heart.Journal of bioenergetics and biomembranes · 2009Review
- Glutathione oxidation as a trigger of mitochondrial depolarization and oscillation in intact hearts.Journal of molecular and cellular cardiology · 2008Article
- Redox-optimized ROS balance: a unifying hypothesis.Biochimica et biophysica actaArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Ca(2+) is well known as the central player in cardiac cell physiology, mediating Ca(2+) activation of myosin ATPase and contraction, the stimulation of Ca(2+)-activated signaling pathways and modulation of mitochondrial energy production. Abnormalities of Ca(2+) handling are a well-studied mechanism of decompensation in heart failure. Less appreciated is the role of cytosolic Na(+) (Na(i) (+)), which can dramatically influence the transfer rates and distribution of Ca(2+) among the intracellular compartments of the myocyte. Since Na(i) (+) can vary widely under different physiological and pathological conditions, and its effects depend on multiple ion gradients and membrane electrical potentials, unraveling the global influence of Na(i) (+) on cell function is complex, requiring an integrative view of cardiomyocyte physiology. Here, we discuss how abnormal Na(i) (+) regulation not only influences the cytosolic Ca(2+) transient and the cellular action potential but also alters mitochondrial Ca(2+) uptake and the balance of energy supply and demand of the cardiomyocyte, which may contribute to oxidative stress and cardiac decompensation. The implications for sudden cardiac death and the potential for novel therapeutic interventions are discussed.
Identifiers
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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.