ArticleThe Journal of clinical investigation1995
Differential regulation of two types of intracellular calcium release channels during end-stage heart failure.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
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.
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Who cites it
82 citing papers in PubMed, 245 citations in OpenAlex.
- Review
- Modeling the spatiotemporal properties of crosstalk between RyR-mediated and IPFrontiers in cell and developmental biology · 2026Article
- Activation of IPAmerican journal of physiology. Heart and circulatory physiology · 2024Article
- Using a Failing Human Ventricular Cardiomyocyte Model to Re-Evaluate CaBiomolecules · 2024Article
- Activation of IPAmerican journal of physiology. Heart and circulatory physiology · 2024Article
- Altering Calcium Sensitivity in Heart Failure: A Crossroads of Disease Etiology and Therapeutic Innovation.International journal of molecular sciences · 2023Review
- Inositol 1,4,5-trisphosphate receptors in cardiomyocyte physiology and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Effects of Sarcolemmal Background CaFrontiers in physiology · 2022Article
- Identifying Features of Cardiac Disease Phenotypes Based on Mechanical Function in a Catecholaminergic Polymorphic Ventricular Tachycardia Model.Frontiers in bioengineering and biotechnology · 2022Article
- D,L-Methadone causes leukemic cell apoptosis via an OPRM1-triggered increase in IP3R-mediated ER CaScientific reports · 2021Article
- Endoplasmic Reticulum-Based Calcium Dysfunctions in Synucleinopathies.Frontiers in neurology · 2021Review
- Crucial Role of Mammalian Glutaredoxin 3 in Cardiac Energy Metabolism in Diet-induced Obese Mice Revealed by Transcriptome Analysis.International journal of biological sciences · 2021Article
- Increases in [IP3]i aggravates diastolic [Ca2+] and contractile dysfunction in Chagas' human cardiomyocytes.PLoS neglected tropical diseases · 2020Article
- Reduced CaAging · 2020Article
- Homocysteine-induced electrical remodeling via the mediation of IPAmerican journal of translational research · 2020Article
- Obstruction of ventricular CaThe Journal of physiology · 2018Article
- Cell death mechanisms of the anti-cancer drug etoposide on human cardiomyocytes isolated from pluripotent stem cells.Archives of toxicology · 2018Article
- Highly variable contractile performance correlates with myocyte content in trabeculae from failing human hearts.Scientific reports · 2018Article
- The role of βII spectrin in cardiac health and disease.Life sciences · 2018Review
- Computational Modeling of Electrophysiology and Pharmacotherapy of Atrial Fibrillation: Recent Advances and Future Challenges.Frontiers in physiology · 2018Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The molecular basis of human heart failure is unknown. Alterations in calcium homeostasis have been observed in failing human heart muscles. Intracellular calcium-release channels regulate the calcium flux required for muscle contraction. Two forms of intracellular calcium-release channels are expressed in the heart: the ryanodine receptor (RyR) and the inositol 1,4,5-trisphosphate receptor (IP3R). In the present study we showed that these two cardiac intracellular calcium release channels were regulated in opposite directions in failing human hearts. In the left ventricle, RyR mRNA levels were decreased by 31% (P < 0.025) whereas IP3R mRNA levels were increased by 123% (P < 0.005). In situ hybridization localized both RyR and IP3R mRNAs to human cardiac myocytes. The relative amounts of IP3 binding sites increased approximately 40% compared with ryanodine binding sites in the failing heart. RyR down-regulation could contribute to impaired contractility; IP3R up regulation may be a compensatory response providing an alternative pathway for mobilizing intracellular calcium release, possibly contributing to the increased diastolic tone associated with heart failure and the hypertrophic response of failing myocardium.
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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.