ArticleBiophysical journal2007
Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger.
Article in Biophysical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed, 67 citations in OpenAlex.
- Regulation of Na/Ca exchange by cytoplasmic protons modifies intracellular calcium dynamics and the cardiac response to ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cardiac Na/Ca Exchange Suppression: A Late-Breaking Knockout Story Showing That There Is No Free Lunch.Journal of the American Heart Association · 2021Article
- Acute Genetic Ablation of Cardiac Sodium/Calcium Exchange in Adult Mice: Implications for Cardiomyocyte Calcium Regulation, Cardioprotection, and Arrhythmia.Journal of the American Heart Association · 2021Article
- New Insights in Cardiac Calcium Handling and Excitation-Contraction Coupling.Advances in experimental medicine and biology · 2018Review
- Distinct Occurrence of Proarrhythmic Afterdepolarizations in Atrial Versus Ventricular Cardiomyocytes: Implications for Translational Research on Atrial Arrhythmia.Frontiers in pharmacology · 2018Article
- Sarcolemmal distribution ofAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Contribution of small conductance KThe Journal of physiology · 2017Article
- The Effects of SEA0400 on CaFrontiers in pharmacology · 2017Article
- Elevated local [Ca2+] and CaMKII promote spontaneous Ca2+ release in ankyrin-B-deficient hearts.Cardiovascular research · 2016Article
- Dysfunction of the β2-spectrin-based pathway in human heart failure.American journal of physiology. Heart and circulatory physiology · 2016Article
- Burst pacemaker activity of the sinoatrial node in sodium-calcium exchanger knockout mice.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Ca²⁺ entry via Trpm2 is essential for cardiac myocyte bioenergetics maintenance.American journal of physiology. Heart and circulatory physiology · 2015Article
- Junctional cleft [Ca²⁺]i measurements using novel cleft-targeted Ca²⁺ sensors.Circulation research · 2014Article
- Role of RyR2 phosphorylation in heart failure and arrhythmias: protein kinase A-mediated hyperphosphorylation of the ryanodine receptor at serine 2808 does not alter cardiac contractility or cause heart failure and arrhythmias.Circulation research · 2014Review
- Rad GTPase deletion increases L-type calcium channel current leading to increased cardiac contraction.Journal of the American Heart Association · 2013Article
- Na/Ca exchange and contraction of the heart.Journal of molecular and cellular cardiology · 2013Review
- Different roles of the cardiac Na+/Ca2+-exchanger in ouabain-induced inotropy, cell signaling, and hypertrophy.American journal of physiology. Heart and circulatory physiology · 2013Article
- Complete atrial-specific knockout of sodium-calcium exchange eliminates sinoatrial node pacemaker activity.PloS one · 2013Article
- Cardiac sodium-calcium exchange and efficient excitation-contraction coupling: implications for heart disease.Advances in experimental medicine and biology · 2013Review
- 20 years from NCX purification and cloning: milestones.Advances in experimental medicine and biology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
L-type Ca2+ current (I(Ca)) is reduced in myocytes from cardiac-specific Na+-Ca2+ exchanger (NCX) knockout (KO) mice. This is an important adaptation to prevent Ca2+ overload in the absence of NCX. However, Ca2+ channel expression is unchanged, suggesting that regulatory processes reduce I(Ca). We tested the hypothesis that an elevation in local Ca2+ reduces I(Ca) in KO myocytes. In patch-clamped myocytes from NCX KO mice, peak I(Ca) was reduced by 50%, and inactivation kinetics were accelerated as compared to wild-type (WT) myocytes. To assess the effects of cytosolic Ca2+ concentration on I(Ca), we used Ba2+ instead of Ca2+ as the charge carrier and simultaneously depleted sarcoplasmic reticular Ca2+ with thapsigargin and ryanodine. Under these conditions, we observed no significant difference in Ba2+ current between WT and KO myocytes. Also, dialysis with the fast Ca2+ chelator BAPTA eliminated differences in both I(Ca) amplitude and decay kinetics between KO and WT myocytes. We conclude that, in NCX KO myocytes, Ca2+-dependent inactivation of I(Ca) reduces I(Ca) amplitude and accelerates current decay kinetics. We hypothesize that the elevated subsarcolemmal Ca2+ that results from the absence of NCX activity inactivates some L-type Ca2+ channels. Modulation of subsarcolemmal Ca2+ by the Na+-Ca2+ exchanger may be an important regulator of excitation-contraction coupling.
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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.