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Proposed mechanism by which OA-NO2 reduces fibrosis in the atrium of AngII-treated mice. OA-NO2 decreases fibroblast transdifferentiation through inhibition of Smad-2 activation, as indicated by a reduction of α-SMA expression. Additionally, OA-NO2 reduces atrial oxidative stress due to attenuation of superoxide production from macrophages and fibroblasts by inhibition of NOX2 and p67 phox expression via p38 MAPK deactivation.
