This study demonstrated that HO-1 expression and activity in ECs are present only in advanced atherosclerosis whereas, VEGF expression is present in early as well as in advanced atherosclerosis and the degree of its expression increases with severity of atherosclerosis.
Elucidation of the molecular mechanisms which control HO-1 gene expression will allow us to develop therapeutic strategies to enhance the cytoprotective potential of HO-1 in atherosclerosis.
These results suggest that the overexpression of introduced hHO-1 is potentially able to reduce the risk factors of atherosclerosis, partially due to its cellular protection against oxidative injury and to its inhibitory effect on cellular proliferation.
Patients with AAA were less frequently carriers of short (< 25 GT) repeats in the HO-1 gene promoter than patients with atherosclerosis or healthy subjects.