| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5556899 | Life Sciences | 2017 | 8 Pages |
Abstract
The transformation of atrial fibroblasts into myofibroblasts through activation of TGF-β1 and CTGF emerged as potential cellular trigger of fibrogenesis. Prevention of fibroblast-to-myofibroblast switching may serve as target for remodeling-based antiarrhythmic AF therapy.
Keywords
ECMTGFLVEFSMADDAPIHDACCTGFGAPDH4′,6-diamidino-2-phenylindolesmooth muscle actinRemodelingtransforming growth factorSMASinus rhythmConnective tissue growth factorFibroblastFibrosisAtrial fibrillationExtracellular matrixAnimal modelMyofibroblastheart failurehistone deacetylaseleft ventricular ejection fractionglyceraldehyde 3-phosphate dehydrogenase
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Authors
Patrick Lugenbiel, Fabian Wenz, Katharina Govorov, Pascal Syren, Hugo A. Katus, Dierk Thomas,