ArticleBritish journal of pharmacology2007
Could Ca2+ sensitizers rescue patients from chronic congestive heart failure?
Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 14 citations in OpenAlex.
- Levosimendan reduces segmental pulmonary vascular resistance in isolated perfused rat lungs and relaxes human pulmonary vessels.PloS one · 2020Article
- Phosphodiesterase inhibitor KMUP-3 displays cardioprotection via protein kinase G and increases cardiac output via G-protein-coupled receptor agonist activity and Ca(2+) sensitization.The Kaohsiung journal of medical sciences · 2016Article
- Crystal structure of cardiac troponin C regulatory domain in complex with cadmium and deoxycholic acid reveals novel conformation.Journal of molecular biology · 2011Article
- A structural and functional perspective into the mechanism of Ca2+-sensitizers that target the cardiac troponin complex.Journal of molecular and cellular cardiology · 2010Article
- Levosimendan induces NO production through p38 MAPK, ERK and Akt in porcine coronary endothelial cells: role for mitochondrial K(ATP) channel.British journal of pharmacology · 2009Article
- Interaction of cardiac troponin with cardiotonic drugs: a structural perspective.Biochemical and biophysical research communications · 2008Review
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Abstract
Attempts to ameliorate cardiac contractile dysfunction by Ca(2+) mobilizers, such as catecholamines, phosphodiesterase (PDE) inhibitors and digitalis, play an important role in pharmacotherapy for congestive heart failure (CHF), but these agents possess disadvantages in causing Ca(2+) overload resulting in arrhythmogenicity and damage to cardiomyocytes. Ca(2+) sensitizers that act directly on contractile proteins are free from the risk of Ca(2+) overload and they could improve haemodynamic parameters with minimum increase in energy expenditure even under pathological conditions, including acidosis and stunned myocardium. Beneficial effects of levosimendan (that acts by combination of Ca(2+) sensitization and PDE inhibition) on CHF due to hypertensive cardiomyopathy in Dahl/Rapp rats as reported in this issue demonstrate the potential of oral levosimendan in long-term treatment of chronic CHF. Since chronic CHF in clinical settings is much more complex, careful analysis of clinical outcomes will be required to establish the therapeutic relevance of Ca(2+) sensitizers in the treatment of chronic CHF.
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