It has been reported that elevation of HO-1 by treatment with cobalt protoporphyrin IX (CoPP IX) or a recombinant adenovirus carrying the human HO-1 gene attenuated cardiac hypertrophy and apoptosis, in both an Ang-II-induced HF model and a spontaneously hypertensive rat model [25, 70], while this pathological process was exacerbated in the presence of tin protoporphyrin, an inhibitor of HO activity [70]. This evidence concerns the gene HMOX1 and hydrops fetalis.