However, the proangiogeniceffects of PPARγ ligands via modulation of the VEGF/VEGF-receptor system (that signalsvia the ERK cascade) have gained recognition (reviewed by [49]), which may be beneficial fortherapy of vascular diseases (e.g., infarction) [135, 136] but detrimental in cancer tissue.For example, in rat myofibroblasts, rosiglitazone and 15-deoxy-Δ(12,14)-PGJ2 induce expression ofVEGF and its receptors (Flt1 and KDR, that signal via the ERK cascade), andaugment tubule formation on a matrigel, indicative of a promoting function ofPPARγ and ERKs in angiogenesis [137]. Here, MAPK1 is linked to infarction.