Consecuencias eléctricas de la fibrosis miocárdica mediada por TGF-βremodelado estructural y desarrollo de fibrilación auricular TGF-B

Laburpena

Sustained pressure overload can elicit in the atrium from patients with severe aortic stenosis a harmful remodeling, which constitutes the substrate for atrial fibrillation (AF) development. Progressive accumulation of fibrotic tissue due to increased expression of extracellular matrix proteins (colagens I-III, fibronectin-1, lisil-oxidase) is the major component of cardiac remodeling. Deregulation of expression of TGF-ß family citoquines is the hallmark of structural remodeling and atrial fibrosis in AF. TGF-ß1 expression in right atrium is significantly increased in patients with severe aortic stenosis and AF, compared to those remaining in sinus rhythm. Interestingly, the TGF-ß1 profibrogenic activity is reinforced by decreased expression of BMP-7 and inhibin. In the same way, the expression of microRNAs miR-1, miR-133 and miR-29, all of them repressing the transcription of genes encoding proteins involved in extracellular matrix turn-over, is downregulated in right atrial tissue of patients with severe aortic stenosis and AF, which may contribute to structural remodeling in this setting.