ArticleIUBMB life2009
Na+ transport in cardiac myocytes; Implications for excitation-contraction coupling.
Article in IUBMB life, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- A model for the human fetal ventricular myocyte electrophysiology.PLoS computational biology · 2026Article
- Calcium Signaling and Cardiac Adaptation to Stress: Focus on Pregnancy and Diabetes.Biomolecules · 2025Review
- Mechanistic Relevance of Ventricular Arrhythmias in Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- Obesity Arrhythmias: Role of IL-6 Trans-Signaling.International journal of molecular sciences · 2024Review
- STAT4 Mediates IL-6 Trans-Signaling Arrhythmias in High Fat Diet Guinea Pig Heart.International journal of molecular sciences · 2024Article
- Comparative cardiotoxicity assessment of bisphenol chemicals and estradiol using human induced pluripotent stem cell-derived cardiomyocytes.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Hypoxic Stress-Dependent Regulation of Na,K-ATPase in Ischemic Heart Disease.International journal of molecular sciences · 2023Review
- Regulation of Cardiac Contractility by the Alpha 2 Subunit of the NaFrontiers in physiology · 2022Review
- Cardioplegia between Evolution and Revolution: From Depolarized to Polarized Cardiac Arrest in Adult Cardiac Surgery.Journal of clinical medicine · 2021Review
- Mechanisms underlying the pathophysiology of heart failure with preserved ejection fraction: the tip of the iceberg.Heart failure reviews · 2021Review
- Long-Chain Acylcarnitines and Cardiac Excitation-Contraction Coupling: Links to Arrhythmias.Frontiers in physiology · 2020Review
- Heart failure leads to altered β2-adrenoceptor/cyclic adenosine monophosphate dynamics in the sarcolemmal phospholemman/Na,K ATPase microdomain.Cardiovascular research · 2019Article
- Cardiolipotoxicity, Inflammation, and Arrhythmias: Role for Interleukin-6 Molecular Mechanisms.Frontiers in physiology · 2018Review
- Hypokalemia-Induced Arrhythmias and Heart Failure: New Insights and Implications for Therapy.Frontiers in physiology · 2018Review
- Cardiac Ion Channel Regulation in Obesity and the Metabolic Syndrome: Relevance to Long QT Syndrome and Atrial Fibrillation.Frontiers in physiology · 2017Review
- Enzyme localization, crowding, and buffers collectively modulate diffusion-influenced signal transduction: Insights from continuum diffusion modeling.The Journal of chemical physics · 2015Article
- Article
- While systolic cardiomyocyte function is preserved, diastolic myocyte function and recovery from acidosis are impaired in CaMKIIδ-KO mice.Journal of molecular and cellular cardiology · 2013Article
- Hyperkalemic cardioplegia for adult and pediatric surgery: end of an era?Frontiers in physiology · 2013Review
- Na⁺/K⁺-ATPase E960 and phospholemman F28 are critical for their functional interaction.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
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 1 country.
Funding
Abstract
Intracellular Na(+) concentration ([Na(+)](i)) is very important in modulating the contractile and electrical activity of the heart. Upon electrical excitation of the myocardium, voltage-dependent Na(+) channels open, triggering the upstroke of the action potential (AP). During the AP, Ca(2+) enters the myocytes via L-type Ca(2+) channels. This triggers Ca(2+) release from the sarcoplasmic reticulum (SR) and thus activates contraction. Relaxation occurs when cytosolic Ca(2+) declines, mainly due to re-uptake into the SR via SR Ca(2+)-ATPase and extrusion from the cell via the Na(+)/Ca(2+) exchanger (NCX). NCX extrudes one Ca(2+) ion in exchange for three Na(+) ions and its activity is critically regulated by [Na(+)](i). Thus, via NCX, [Na(+)](i) is centrally involved in the regulation of intracellular [Ca(2+)] and contractility. Na(+) brought in by Na(+) channels, NCX and other Na(+) entry pathways is extruded by the Na(+)/K(+) pump (NKA) to keep [Na(+)](i) low. NKA is regulated by phospholemman, a small sarcolemmal protein that associates with NKA. Unphosphorylated phospholemman inhibits NKA by decreasing the pump affinity for internal Na(+) and this inhibition is relieved upon phosphorylation. Here we discuss the main characteristics of the Na(+) transport pathways in cardiac myocytes and their physiological and pathophysiological relevance.
Identifiers
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.