In line with p53 accumulation during cardiac hypertrophy, pressure overload is associated with increased cardiac expression of TSP1 (253) and TSP4 (254), and the differential expression of proangiogenic (e.g., VEGF) and antiangiogenic (e.g., TSP1) growth factors in the hypertrophied heart during chronic hypoxia may contribute to the suppressed angiogenesis observed during late stages of cardiac hypertrophy, as suggested by findings in a rat model of angiotensin II-induced cardiac hypertrophy and heart failure (255). This evidence concerns the gene TP53 and heart failure.