Inflammatory activation of human cardiac fibroblasts leads to altered calcium signaling, decreased connexin 43 expression and increased glutamate secretion
@article{Skildebrand2017InflammatoryAO, title={Inflammatory activation of human cardiac fibroblasts leads to altered calcium signaling, decreased connexin 43 expression and increased glutamate secretion}, author={Eva Ski{\"o}ldebrand and Annika Lundqvist and Ulrika Björklund and Mikael Sandstedt and Anders Lindahl and Elisabeth Hansson and Lillemor Mattsson Hult{\'e}n}, journal={Heliyon}, year={2017}, volume={3} }
10 Citations
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- Biology, MedicineCells
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- BiologyScandinavian journal of pain
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- Medicine, BiologyPloS one
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- Biology, MedicineMolecular and Cellular Biochemistry
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References
SHOWING 1-10 OF 46 REFERENCES
Cardiac fibroblasts: at the heart of myocardial remodeling.
- BiologyPharmacology & therapeutics
- 2009
Cardiac fibroblasts support cardiac inflammation in heart failure
- Biology, MedicineBasic Research in Cardiology
- 2014
It is found that mechanical stretch mimicking cardiac dilation in heart failure induces activation of fibroblasts and not only stimulates production of extracellular matrix but more interestingly up-regulates chemokine production and triggers typical inflammatory pathways in vitro.
Myocardial fibroblast-matrix interactions and potential therapeutic targets.
- Medicine, BiologyJournal of molecular and cellular cardiology
- 2014
Cross talk between cardiac myocytes and fibroblasts: from multiscale investigative approaches to mechanisms and functional consequences.
- BiologyAmerican journal of physiology. Heart and circulatory physiology
- 2012
Targeting cross talk between CM and CF could potentially be used therapeutically for the modulation of the cardiac remodeling response in the diseased heart and may lead to new strategies for the treatment of heart failure or rhythm disturbances.
Effects of interleukin-1 on cardiac fibroblast function: relevance to post-myocardial infarction remodelling.
- Biology, MedicineVascular pharmacology
- 2014
Reduced heterogeneous expression of Cx43 results in decreased Nav1.5 expression and reduced sodium current that accounts for arrhythmia vulnerability in conditional Cx43 knockout mice.
- Biology, MedicineHeart rhythm
- 2012
Upregulation of the 5-Lipoxygenase Pathway in Human Aortic Valves Correlates With Severity of Stenosis and Leads to Leukotriene-Induced Effects on Valvular Myofibroblasts
- Medicine, BiologyCirculation
- 2011
The upregulation of the LT pathway in human aortic valve stenosis and its correlation with clinical stenosis severity, taken together with the potentially detrimental LT-induced effects on valvular myofibroblasts, suggests one possible role of inflammation in the development of aorta stenosis.
Mitogenic and secretory responses of human valve interstitial cells to vasoactive agents.
- Biology, MedicineThe Journal of heart valve disease
- 2000
It is shown that 5-HT and Ang II promote the prolonged processes of growth and collagen synthesis in cultured human valve IC, thus, these vasoactive agents may play a role in the development of heart valve disease.
Characteristics of agonist-induced Ca2+ responses in diseased human valvular myofibroblasts.
- Biology, MedicineProceedings of the Western Pharmacology Society
- 2008
Ca2+ responses induced by different agonists in normal and rheumatic VMFs are examined to provide information pertaining to Ca2+-associated changes and their consequences in cardiac valvular diseases.
Single-target RNA interference for the blockade of multiple interacting proinflammatory and profibrotic pathways in cardiac fibroblasts.
- BiologyJournal of molecular and cellular cardiology
- 2014