In the human scenario, circumstantial evidence suggestive for a contribution of TGF-β1 from a plasmatic source to pressure overload myocardial remodeling was provided by some reports showing that TGF-β1 plasma levels are increased in hypertensive patients, with or without metabolic syndrome [14] with target organ damage, including heart hypertrophy [15], [16]. Here, TGFB1 is linked to metabolic syndrome.