Polymorphic Causes of Atherosclerosis

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Polymorphic Causes of Atherosclerosis

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Polymorphic Causes of Atherosclerosis

Introduction

Guzik et al. (2000) argued that the role of oxidative stress in the pathogenesis of vascular diseases such as atherosclerosis is critical. The increase in superoxide anion production causes an increase in the oxidative stress and reduces the bioactivity of nitric oxide in vascular diseases. The role of NAD(P)H oxidase as a source of superoxide anions is of great significance and one of its subunit p22phox is predominantly expressed in different coronary disorders. It has been established in the preliminary research studies that a possible association exists between atherosclerosis and the polymorphism seen in the p22phox residue of CYBA gene encoding NAD (P) H oxidase. The researchers tested their relationship by examining the relationship between CYBA C242T polymorphism and the levels of superoxide generation in the blood vessels of humans.

Ishigami et al. (1995) have worked on the connection between the polymorphism of angiotensin-converting enzyme (ACE) gene and different cardiovascular diseases such as coronary atherosclerosis. The plasma activity of ACE has been related to the carotid-wall thickening. Many researchers have postulated that exposure to raised levels of plasma ACE on a long-term basis can cause structural changes in the vessel walls. It has been postulated that preeclampsia and essential hypertension are linked with mutation in the genes encoding angiotensin. These facts reflect that renin-angiotensin system might be involved in advancement of cardiovascular diseases. The study considered the role of molecular variants of the angiotensinogen gene as a genetic cause of coronary atherosclerosis. The researchers analyzed used polymerase chain reaction (PCR) to find the point mutations in the angiotensinogen gene. The frequencies of these alleles were compared in atherosclerotic patients as well as the control subjects.

Zhang et al. (1999) studied the polymorphism of Gelatinase B, a type of matrix metalloproteinase possessing proteolytic properties against the proteins in the connective tissue. Gelatinase B is of particular significance in the remodeling procedures in the connective tissue and previous studies have associated it with atherogenesis as well as the rupture of plaque. It possesses a broad substrate specificity and is the most active against type IV collagen, gelatin, elastin and the proteoglycan core proteins. The study hypothesized that the variation in base sequence within the promoter region of gelatinase B can alter its level. This alteration is capable of affecting the degradation of connective tissue during atherogenesis and the lesion progression. This can predispose the people carrying genetic variants to a more severe form of atherosclerosis.