ArticleJournal of muscle research and cell motility2010
More severe cellular phenotype in human idiopathic dilated cardiomyopathy compared to ischemic heart disease.
Article in Journal of muscle research and cell motility, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Sarcomere length affects Ca2+ sensitivity of contraction in ischemic but not non-ischemic myocardium.The Journal of general physiology · 2023Article
- Article
- Titin-truncating mutations associated with dilated cardiomyopathy alter length-dependent activation and its modulation via phosphorylation.Cardiovascular research · 2022Article
- Cardiac sarcomere mechanics in health and disease.Biophysical reviews · 2021Review
- De Novo Missense Mutations inInternational journal of molecular sciences · 2021Article
- Heart Failure in Humans Reduces Contractile Force in Myocardium From Both Ventricles.JACC. Basic to translational science · 2020Article
- Troponin destabilization impairs sarcomere-cytoskeleton interactions in iPSC-derived cardiomyocytes from dilated cardiomyopathy patients.Scientific reports · 2020Article
- Biomarkers for Heart Failure Prognosis: Proteins, Genetic Scores and Non-coding RNAs.Frontiers in cardiovascular medicine · 2020Review
- Phosphorylation Modifications Regulating Cardiac Protein Quality Control Mechanisms.Frontiers in physiology · 2020Review
- Posttranslational modifications of calcium/calmodulin-dependent protein kinase IIδ and its downstream signaling in human failing hearts.American journal of translational research · 2017Article
- S-glutathiolation impairs phosphoregulation and function of cardiac myosin-binding protein C in human heart failure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- The Frank-Starling mechanism involves deceleration of cross-bridge kinetics and is preserved in failing human right ventricular myocardium.American journal of physiology. Heart and circulatory physiology · 2015Article
- A novel phosphorylation site, Serine 199, in the C-terminus of cardiac troponin I regulates calcium sensitivity and susceptibility to calpain-induced proteolysis.Journal of molecular and cellular cardiology · 2015Article
- LKB1/Mo25/STRAD uniquely impacts sarcomeric contractile function and posttranslational modification.Biophysical journal · 2015Article
- Troponin I phosphorylation in human myocardium in health and disease.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2014Article
- Phosphorylation of protein kinase C sites Ser42/44 decreases Ca(2+)-sensitivity and blunts enhanced length-dependent activation in response to protein kinase A in human cardiomyocytes.Archives of biochemistry and biophysics · 2014Article
- Transmural heterogeneity of cellular level power output is reduced in human heart failure.Journal of molecular and cellular cardiology · 2014Article
- RNA-sequencing analysis reveals new alterations in cardiomyocyte cytoskeletal genes in patients with heart failure.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Length-dependent activation is modulated by cardiac troponin I bisphosphorylation at Ser23 and Ser24 but not by Thr143 phosphorylation.American journal of physiology. Heart and circulatory physiology · 2014Article
- Role of STAT3 in angiotensin II-induced hypertension and cardiac remodeling revealed by mice lacking STAT3 serine 727 phosphorylation.Hypertension research : official journal of the Japanese Society of Hypertension · 2013Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the β-adrenergic receptor (βAR) pathway is the main mechanism of the heart to increase cardiac output via protein kinase A (PKA)-mediated phosphorylation of cellular target proteins, and perturbations therein may contribute to cardiac dysfunction in heart failure. In the present study a comprehensive analysis was made of mediators of the βAR pathway, myofilament properties and cardiac structure in patients with idiopathic (IDCM; n = 13) and ischemic (ISHD; n = 10) cardiomyopathy in comparison to non-failing hearts (donor; n = 10) for the following parameters: βAR density, G-coupled receptor kinases 2 and 5, stimulatory and inhibitory G-proteins, phosphorylation of myofilament targets of PKA, protein phosphatase 1, phospholamban, SERCA2a and single myocyte contractility. All parameters exhibited the expected alterations of heart failure, but for most of them the extent of alteration was greater in IDCM than in ISHD. Histological analysis also revealed higher collagen in IDCM compared to ISHD. Alterations in the βAR pathway are more pronounced in IDCM than in ISHD and may reflect sequential changes in cellular protein composition and function. Our data indicate that cellular dysfunction is more severe in IDCM than in ISHD.
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