ArticleCirculation research2008
Ca2+ influx through T- and L-type Ca2+ channels have different effects on myocyte contractility and induce unique cardiac phenotypes.
Article in Circulation research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed, 73 citations in OpenAlex.
- Electrophysiological Mechanisms and Therapeutic Potential of Calcium Channels in Atrial Fibrillation.Reviews in cardiovascular medicine · 2025Review
- Molecular Regulation of Cardiomyocyte Maturation.Current cardiology reports · 2025Review
- Role of sonic hedgehog signaling pathway in the regulation of ion channels: focus on its association with cardio-cerebrovascular diseases.Journal of physiology and biochemistry · 2023Review
- Evidence for a Physiological Role of T-Type Ca Channels in Ventricular Cardiomyocytes of Adult Mice.Membranes · 2022Article
- A low voltage activated CaChannels (Austin, Tex.) · 2020Article
- A compartmentalized mathematical model of mouse atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020Article
- Berberine Mediated Positive Inotropic Effects on Rat HeartsFrontiers in pharmacology · 2020Article
- Current methods for the maturation of induced pluripotent stem cell-derived cardiomyocytes.World journal of stem cells · 2019Review
- Drosophila Voltage-Gated Calcium Channel α1-Subunits Regulate Cardiac Function in the Aging Heart.Scientific reports · 2018Article
- Increasing T-type calcium channel activity by β-adrenergic stimulation contributes to β-adrenergic regulation of heart rates.The Journal of physiology · 2018Article
- Functional Microdomains in Heart's Pacemaker: A Step Beyond Classical Electrophysiology and Remodeling.Frontiers in physiology · 2018Review
- Negatively charged residues in the first extracellular loop of the L-type CaThe Journal of biological chemistry · 2017Article
- Peptidyl-Prolyl Isomerase 1 Regulates CaJournal of the American Heart Association · 2017Article
- Tetrodotoxin-sensitive Ca2+ Currents, but No T-type Currents in Normal, Hypertrophied, and Failing Mouse Cardiomyocytes.Journal of cardiovascular pharmacology · 2016Article
- Endostatin is protective against monocrotaline-induced right heart disease through the inhibition of T-type Ca(2+) channel.Pflugers Archiv : European journal of physiology · 2016Article
- A mouse model for adult cardiac-specific gene deletion with CRISPR/Cas9.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Endostatin inhibits T-type Ca2+ channel current in guinea pig ventricular myocyte.The Journal of veterinary medical science · 2015Article
- Eps15 Homology Domain-containing Protein 3 Regulates Cardiac T-type Ca2+ Channel Targeting and Function in the Atria.The Journal of biological chemistry · 2015Article
- Microdomain-specific localization of functional ion channels in cardiomyocytes: an emerging concept of local regulation and remodelling.Biophysical reviews · 2015Article
- Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction.Circulation research · 2014Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
T-type Ca(2+) channels (TTCCs) are expressed in the developing heart, are not present in the adult ventricle, and are reexpressed in cardiac diseases involving cardiac dysfunction and premature, arrhythmogenic death. The goal of this study was to determine the functional role of increased Ca(2+) influx through reexpressed TTCCs in the adult heart. A mouse line with cardiac-specific, conditional expression of the alpha1G-TTCC was used to increase Ca(2+) influx through TTCCs. alpha1G hearts had mild increases in contractility but no cardiac histopathology or premature death. This contrasts with the pathological phenotype of a previously studied mouse with increased Ca(2+) influx through the L-type Ca(2+) channel (LTCC) secondary to overexpression of its beta2a subunit. Although alpha1G and beta2a myocytes had similar increases in Ca(2+) influx, alpha1G myocytes had smaller increases in contraction magnitude, and, unlike beta2a myocytes, there were no increases in sarcoplasmic reticulum Ca(2+) loading. Ca(2+) influx through TTCCs also did not induce normal sarcoplasmic reticulum Ca(2+) release. alpha1G myocytes had changes in LTCC, SERCA2a, and phospholamban abundance, which appear to be adaptations that help maintain Ca(2+) homeostasis. Immunostaining suggested that the majority of alpha1G-TTCCs were on the surface membrane. Osmotic shock, which selectively eliminates T-tubules, induced a greater reduction in L- versus TTCC currents. These studies suggest that T- and LTCCs are in different portions of the sarcolemma (surface membrane versus T-tubules) and that Ca(2+) influx through these channels induce different effects on myocyte contractility and lead to distinct cardiac phenotypes.
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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.