Figure 7.

Schematic representation of the FK506 effects on cardiac fibroblasts and endothelial cells under chronic pressure overload conditions. We propose that FK506 rebalances TGFβ/BMP signaling directly in the pressure-overloaded right ventricle by increasing BMP signaling, efficiently reduces collagen production and proliferation of cardiac fibroblasts, and inhibits the rare event of endothelial fate conversion, leading to reduced RV fibrosis, preserved RV capillarization, and, most importantly, better RV function. Red arrows pointing up mean increased. Red arrows pointing down mean decreased.