Moreover, Gal-3 overexpression preceded the onset of HF in failure-prone rats [1], which supports the notion that Gal-3 might accelerate the transition from compensated hypertrophy into overt HF by the stimulation of perivascular and interstitial myocardial fibrosis via the TGF-β/Smad3 signaling pathway [47,48]. This evidence concerns the gene SMAD3 and hydrops fetalis.