Angiotensin II-mediated up-regulation of connective tissue growth factor promotes atrial tissue fibrosis in the canine atrial fibrillation model
Olmesartan
DOI:
10.1093/europace/eus052
Publication Date:
2012-03-28T00:56:13Z
AUTHORS (8)
ABSTRACT
Remodelling of the extracellular matrix (ECM) plays an important role in production arrhythmogenic substrate for atrial fibrillation (AF), and is considered to be promoted by connective tissue growth factor (CTGF).Our objective was assess relationship between CTGF ECM synthesis, effect olmesartan on these processes. Methods resultsFifteen canine AF models were produced rapid stimulation.They divided into three groups: pacing control (n ¼ 5): 6-week pacing, + with (2 mg/kg/day), nonpacing group 5).In group, messenger ribonucleic acid expressions collagen types 1 3 up-regulated comparison non-pacing (P , 0.05) while transforming factor-b (TGF-b) did not exhibit a significant difference.In up-regulations suppressed 0.05).In fluorescent immunostaining, expression localized cytoplasm.The protein level type increased it group. ConclusionsCTGF associated genes atria appearance fibrosis.Because this up-regulation independent TGF-b olmesartan, mediated angiotensin II.
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