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physiological and pathological processes in cardiovascular system. The PPAR receptors
are found to play a significant role in the control of cardiac energy utilization,
metabolism, inflammation and atherogenesis (Barger and Kelly 2000; Marx et al. L999;
Moreno and Fuster 2004). In vivo studies in both human and animal models PPAR "f was
found to be expressed in atherosclerotic regions (Marx et al. 1998; Ricote et al. 1998;
Tontonoz et al. 1998). The increased expression of PPAR I was specifically found in
macrophages, endothelial cells and intimal media smooth muscle cell in atherosclerotic
vessels (Bishop-Bailey 2000). The usage of troglítazone, a potent PPAR 1 agonist, was
shown to prevent the in vitro vascular smooth muscle cell proliferation and migration
which results in the protection against restenosis after balloon angioplasty (Law RE and
Meehan V/ et al. 1996). The usage of PPAR 1 agonist was found to cause the plaque
stabilization in diabetic atherosclerosis thus preventing the occurrence of embolism
(Moreno and Fuster 2004). The usage of different PPAR T was able to reduce the infarct
size induced by regional myocardial ischemia and reperfusion in anesthetized rats
(Thiemermann and Wayman 2001; Wayman et aL.2002). A reduction of infract size by
pretreatment with PPAR 7 agonist was accompanied by the reduction in MCP-I and
ICAM-1 mRNA expression (Ito et al. 2003). Treatment with rosiglitazone was also found
to cause the decrease in the caspase 3 activity and lower the frequency of apoptosis in
cardiac myocytes in hypercholesterolemic rabbits exposed to ischemia/ reperfusion (Liu
et al. 2004). A same study has reported that the protection by rosiglitazone was also
characterized by the attenuation of ischemia-induced increase in p38 and ERK 1/2
activity (Liu et al. 2004). Progression of ventricular hypertrophy was found to be
associated with the downregulation of PPAR a activity (Barger et al. 2000; Sack et al.
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