By A. Squeri
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Additional info for Coronary Artery Disease - New Insights, Novel Apprs.
Moreover, the level of the signalling message may be influenced by changes in the amount of target protein produced in different patients. All these factors could be due to sequence variations in human genes. With respect to cardiovascular disease per se, statins are probably the most frequently prescribed class of drug, and understandably great effort has been invested in trying to understand the genetics of variations in patient response as well as toxicity of these drugs. To begin with, the fact that considerable interindividual variation exists in response to statin therapy, in terms of both lipid-lowering and adverse drug reactions has been demonstrated in several candidate gene studies as well as meta-analyses from several primary and secondary intervention studies.
The human PON1 is an HDLassociated arylesterase that hydrolyzes paraoxon103. It is thought to exert an antiatherogenic effect by protecting LDLs against oxidation104,105 partly by slowing down the accumulation of lipid peroxides in LDLs under oxidizing conditions. Understandably therefore, alterations in the PON1 gene are implicated in dyslipidaemic disorders. Furthermore, free radical production in the immediate postrecanalization phase after thrombotic occlusion of a major coronary artery in humans is associated with MI106.
They not only control lipid metabolism, but also regulate vascular diseases, such as atherosclerosis and hypertension, as well as the expression of genes involved in fatty acid β-oxidation. Specifically, PPAR-γ plays a critical role in adipocyte differentiation and serves as the receptor for the glitazone class of insulin-sensitizing drugs used in the treatment of T2DM. PPARβ polymorphisms are associated with plasma lipid levels, body mass index and the risk for diabetes and CAD88. PPARγ2 variants have also been shown to influence insulin sensitivity in interaction with ADIPOQ or to influence plasma ADIPOQ levels.