ReviewJournal of molecular medicine (Berlin, Germany)2007
Tuning cardiac performance in ischemic heart disease and failure by modulating myofilament function.
Review in Journal of molecular medicine (Berlin, Germany), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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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
19 citing papers in PubMed, 35 citations in OpenAlex.
- TnI Structural Interface with the N-Terminal Lobe of TnC as a Determinant of Cardiac Contractility.Biophysical journal · 2018Article
- Myofilament function and body mass index.Biomedical reports · 2017Article
- 0.9% saline is neither normal nor physiological.Journal of Zhejiang University. Science. B · 2016Review
- Modifications of myofilament protein phosphorylation and function in response to cardiac arrest induced in a swine model.Frontiers in physiology · 2015Article
- Gene transfer into cardiac myocytes.Methods in molecular biology (Clifton, N.J.) · 2015Article
- Maternal diet-induced obesity programs cardiovascular dysfunction in adult male mouse offspring independent of current body weight.Endocrinology · 2014Article
- Ca++-sensitizing mutations in troponin, P(i), and 2-deoxyATP alter the depressive effect of acidosis on regulated thin-filament velocity.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- Mechanisms of altered Ca²⁺ handling in heart failure.Circulation research · 2013Review
- Structural dynamics of muscle protein phosphorylation.Journal of muscle research and cell motility · 2012Review
- pH-responsive titratable inotropic performance of histidine-modified cardiac troponin I.Biophysical journal · 2012Article
- Generation and functional characterization of knock-in mice harboring the cardiac troponin I-R21C mutation associated with hypertrophic cardiomyopathy.The Journal of biological chemistry · 2012Article
- Age and ovariectomy abolish beneficial effects of female sex on rat ventricular myocytes exposed to simulated ischemia and reperfusion.PloS one · 2012Article
- Recent insights into muscle fatigue at the cross-bridge level.Frontiers in physiology · 2012Article
- Pathogenic peptide deviations support a model of adaptive evolution of chordate cardiac performance by troponin mutations.Physiological genomics · 2010Article
- What we know and do not know about sex and cardiac disease.Journal of biomedicine & biotechnology · 2010Review
- Green tea extract protects rats against myocardial infarction associated with left anterior descending coronary artery ligation.Pflugers Archiv : European journal of physiology · 2009Article
- Single histidine button in cardiac troponin I sustains heart performance in response to severe hypercapnic respiratory acidosis in vivo.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Molecular cardiology in translation: gene, cell and chemical-based experimental therapeutics for the failing heart.Journal of cardiovascular translational research · 2008Review
- Role and possible mechanisms of clenbuterol in enhancing reverse remodelling during mechanical unloading in murine heart failure.Cardiovascular research · 2008Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cardiac myofilaments are composed of highly ordered arrays of proteins that coordinate cardiac contraction and relaxation in response to the rhythmic waves of [Ca(2+)] during the cardiac cycle. Several cardiac disease states are associated with altered myofilament protein interactions that contribute to cardiac dysfunction. During acute myocardial ischemia, the sensitivity of the myofilaments to activating Ca(2+) is drastically reduced, largely due to the effects of intracellular acidosis on the contractile machinery. Myofilament Ca(2+) sensitivity remains compromised in post-ischemic or "stunned" myocardium even after complete restoration of blood flow and intracellular pH, likely because of covalent modifications of or proteolytic injury to contractile proteins. In contrast, myofilament Ca(2+) sensitivity can be increased in chronic heart failure, owing in part to decreased phosphorylation of troponin I, the inhibitory subunit of the troponin regulatory complex. We highlight, in this paper, the central role of the myofilaments in the pathophysiology of each of these distinct disease entities, with a particular focus on the molecular switch protein troponin I. We also discuss the beneficial effects of a genetically engineered cardiac troponin I, with a histidine button substitution at C-terminal residue 164, for a variety of pathophysiologic conditions, including hypoxia, ischemia, ischemia-reperfusion and chronic heart failure.
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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.