ReviewThe Journal of physiology2003
Heart failure -- a challenge to our current concepts of excitation-contraction coupling.
Review in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 62 citations in OpenAlex.
- Using a Failing Human Ventricular Cardiomyocyte Model to Re-Evaluate CaBiomolecules · 2024Article
- Detecting heart failure from B-mode ultrasound characterization of arterial pulse waves.American journal of physiology. Heart and circulatory physiology · 2024Article
- PGC-1α deficiency reveals sex-specific links between cardiac energy metabolism and EC-coupling during development of heart failure in mice.Cardiovascular research · 2022Article
- Stress-driven cardiac calcium mishandling via a kinase-to-kinase crosstalk.Pflugers Archiv : European journal of physiology · 2021Review
- Constitutive inhibitory G protein activity upon adenylyl cyclase-dependent cardiac contractility is limited to adenylyl cyclase type 6.PloS one · 2019Article
- Arrhythmogenic and metabolic remodelling of failing human heart.The Journal of physiology · 2016Review
- Altered calsequestrin glycan processing is common to diverse models of canine heart failure.Molecular and cellular biochemistry · 2013Article
- MCARD-mediated gene transfer of GRK2 inhibitor in ovine model of acute myocardial infarction.Journal of cardiovascular translational research · 2013Article
- Transmural heterogeneity and remodeling of ventricular excitation-contraction coupling in human heart failure.Circulation · 2011Article
- Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.American journal of physiology. Heart and circulatory physiology · 2010Article
- Hypersensitivity of excitation-contraction coupling in dystrophic cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2009Article
- Transgenic simulation of human heart failure-like L-type Ca2+-channels: implications for fibrosis and heart rate in mice.Cardiovascular research · 2009Article
- Regulation of excitation-contraction coupling in mouse cardiac myocytes: integrative analysis with mathematical modelling.BMC physiology · 2009Article
- A novel steroid-like compound F90927 exerting positive-inotropic effects in cardiac muscle.British journal of pharmacology · 2006Article
- The L-type calcium channel in the heart: the beat goes on.The Journal of clinical investigation · 2005Review
- Excitation-contraction coupling gain and cooperativity of the cardiac ryanodine receptor: a modeling approach.Biophysical journal · 2005Article
- Altered intracellular Ca2+ handling in heart failure.The Journal of clinical investigation · 2005Review
- Normal and pathological excitation-contraction coupling in the heart -- an overview.The Journal of physiology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Development of novel therapeutic strategies for congestive heart failure (CHF) seems to be hampered by insufficient knowledge of the molecular machinery of excitation-contraction (EC) coupling in both normal and failing hearts. Cardiac hypertrophy and failure represent a multitude of cardiac phenotypes, and available invasive and non-invasive techniques, briefly reviewed here, allow proper quantification of myocardial function in experimental models even in rats and mice. Both reduced fractional shortening and reduced velocity of contraction characterize myocardial failure. Only when myocardial function is depressed in vivo can meaningful studies be done in vitro of contractility and EC coupling. Also, we point out potential limitations with the whole cell patch clamp technique. Two main factors stand out as explanations for myocardial failure. First, a basic feature of CHF seems to be a reduced Ca(2+) load of the sarcoplasmic reticulum (SR) mainly due to a low phosphorylation level of phospholamban. Second, there seems to be a defect of the trigger mechanism of Ca(2+) release from the SR. We argue that this defect only becomes manifest in the presence of reduced Ca(2+) reuptake capacity of the SR and that it may not be solely attributable to reduced gain of the Ca(2+)-induced Ca(2+) release (CICR). We list several possible explanations for this defect that represent important avenues for future research.
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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.