ArticleThe Journal of physiology2010
Cardiomyocytes with disrupted CFTR function require CaMKII and Ca(2+)-activated Cl(-) channel activity to maintain contraction rate.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed, 50 citations in OpenAlex.
- MITF Regulates CFTR Expression to Participate in Myocardial Ischemia-Reperfusion Injury.The journal of gene medicine · 2026Article
- A Non-Channel Function of CFTR: Attenuating Mitochondrial Oxidative Stress and Cardiomyocyte Senescence via Stabilization by USP45.Aging cell · 2026Article
- Beyond the mutations: spatiotemporal regulation of CFTR by cAMP and calcium signaling in epithelial physiology and cystic fibrosis.Cellular & molecular biology letters · 2025Review
- Can Bioactive Food Substances Contribute to Cystic Fibrosis-Related Cardiovascular Disease Prevention?Nutrients · 2023Review
- Cardiac involvement in cystic fibrosis evaluated using cardiopulmonary magnetic resonance.The international journal of cardiovascular imaging · 2022Article
- Review
- Cystic Fibrosis Transmembrane Conductance Regulator Genotype, Not Circulating Catecholamines, Influences Cardiovascular Function in Patients with Cystic Fibrosis.Clinical medicine insights. Circulatory, respiratory and pulmonary medicine · 2019Article
- Subclinical Left Ventricular Dysfunction is Influenced by Genotype Severity in Patients with Cystic Fibrosis.Clinical medicine insights. Circulatory, respiratory and pulmonary medicine · 2018Article
- Exercise Stroke Volume in Adult Cystic Fibrosis: A Comparison of Acetylene Pulmonary Uptake and Oxygen Pulse.Clinical medicine insights. Circulatory, respiratory and pulmonary medicine · 2018Article
- Proteostasis in cardiac health and disease.Nature reviews. Cardiology · 2017Review
- CaMKII: The molecular villain that aggravates cardiovascular disease.Experimental and therapeutic medicine · 2017Article
- The impact of Cystic Fibrosis Transmembrane Regulator Disruption on cardiac function and stress response.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2016Article
- Role of CaMKII in cardiac arrhythmias.Trends in cardiovascular medicine · 2015Review
- Susceptibility of murine induced pluripotent stem cell-derived cardiomyocytes to hypoxia and nutrient deprivation.Stem cell research & therapy · 2015Article
- Genotype-specific alterations in vascular smooth muscle cell function in cystic fibrosis piglets.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2014Article
- Genetically encoded fluorescent biosensors for live-cell visualization of protein phosphorylation.Chemistry & biology · 2014Review
- Article
- Pulmonary hypertension survival effects and treatment options in cystic fibrosis.Current opinion in pulmonary medicine · 2013Review
- Left ventricular and aortic dysfunction in cystic fibrosis mice.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2013Article
- MRP4 and CFTR in the regulation of cAMP and β-adrenergic contraction in cardiac myocytes.European journal of pharmacology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The physiological role of the cystic fibrosis transmembrane conductance regulator (CFTR) in cardiomyocytes remains unclear. Using spontaneously beating neonatal ventricular cardiomyocytes from wild-type (WT) or CFTR knockout (KO) mice, we examined the role of CFTR in the modulation of cardiomyocyte contraction rate. Contraction rates of spontaneously beating myocytes were captured by video imaging. Real-time changes in intracellular ([Ca(2+)](i)) and protein kinase A (PKA) activity were measured by fura-2 and fluorescence resonance energy transfer, respectively. Acute inhibition of CFTR in WT cardiomyocytes using the CFTR inhibitor CFTR(inh)-172 transiently inhibited the contraction rate. By contrast, cardiomyocytes from CFTR KO mice displayed normal contraction rates. Further investigation revealed that acute inhibition of CFTR activity in WT cardiomyocytes activated L-type Ca(2+) channels, leading to a transient increase of [Ca(2+)](i) and inhibition of PKA activity. Additionally, we found that contraction rate normalization following acute CFTR inhibition in WT cardiomyocytes or chronic deletion in cardiomyocytes from CFTR KO mice requires the activation of Ca(2+)/calmodulin-dependent kinase II (CaMKII) and Ca(2+)-activated Cl(-) channels (CaCC) because simultaneous addition of myristoylated-autocamtide-2-related inhibitory peptide or niflumic acid and CFTR(inh)-172 to WT cardiomyocytes or treatment of cardiomyoctes from CFTR KO mice with these agents caused sustained attenuation of contraction rates. Our results demonstrate that regulation of cardiomyocyte contraction involves CFTR. They also reveal that activation of CaMKII and CaCC compensates for loss of CFTR function. Increased dependence on CaMKII upon loss of CFTR function might leave cystic fibrosis patients at increased risk of heart dysfunction and disease.
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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.