Pharmacological activation of peroxisome proliferator-activated receptor gamma (PPAR¿) has been shown to attenuate pressure overload-induced cardiac fibrosis, suggesting that PPAR¿ has an antifibrotic effect. This study tested the hypothesis that there is a functional interaction between transforming growth factor-ß (TGF-ß) signaling and endogenous PPAR¿ expression in cardiac fibroblasts and pressure overloaded heart.

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