Oxidative stress and atherosclerosis

Singh, U. S.; Jialal, Ishwarlal

doi:10.1016/j.pathophys.2006.05.002

Cited by 407 publications

(296 citation statements)

References 130 publications

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“…Myocardial infarction, stroke or sudden cardiac death are the fatal end-points of progressive atherosclerosis and are thought to be the result of these pathological remodelling processes. 39,40,41,42 According to the theory of oxidative stress, atherosclerosis is the result of the oxidative modification of low density lipoproteins (LDL) in the arterial wall by reactive oxygen species (ROS), from the endothelial cells, macrophages, smooth muscle cells and the adventitial cells. The increased production of ROS reduces the production and consequently the bioavailability of NO, leading to vasoconstriction, platelet aggregation and adhesion of neutrophils to the endothelium.…”

Section: Atherosclerosis and Oxidative Stressmentioning

confidence: 99%

Role of Ace Inhibitors In Atherosclerosis

Shafi

2013

Int J of Biomed & Adv Res

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Section: Atherosclerosis and Oxidative Stressmentioning

confidence: 99%

Role of Ace Inhibitors In Atherosclerosis

Shafi

2013

Int J of Biomed & Adv Res

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“…Furthermore, the management of cardiovascular disease (CVD) is an important issue in cases of chronic renal failure (CRF) patients, and oxidative stress has been speculated to greatly contribute to such onset (2,3). However, the development of effective treatment methods for reducing oxidative stress has also been sought on behalf of CRF.…”

Section: Introductionmentioning

confidence: 99%

An Oral Adsorbent, AST-120 Protects Against the Progression of Oxidative Stress by Reducing the Accumulation of Indoxyl Sulfate in the Systemic Circulation in Renal Failure

Shimoishi

Anraku²,

Kitamura³

et al. 2007

Pharm Res

104

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Purpose. The effect of AST-120, an oral adsorbent, on oxidative stress in the systemic circulation in chronic renal failure (CRF) was examined and the potential role of indoxyl sulfate (IS), an uremic toxin adsorbed by AST-120, in inducing the formation of reactive oxygen species (ROS) in the vascular system was studied, in vitro and in vivo. Materials and methods. The level of oxidized albumin, a marker for oxidative stress in the systemic circulation was determined by HPLC, as previously reported. The mRNA levels of TGF-b 1 and Oat1 were measured by quantitative RT-PCR. The IS induced ROS generation in cultured human umbilical vein endothelial cells (HUVECs) was estimated using a fluorescence microplate reader.Results. An increase in the ratio of oxidized to unoxidized albumin was determined using 5/6 nephrectomized rats (CRF rats) compared to a control group. The ratio was significantly reduced in the group that received AST-120 of 4 weeks, suggesting that AST-120 inhibits oxidative stress in CRF. An anti-oxidative effect of AST-120 was also observed in CRF rats with a similar renal function. The ratio of oxidized albumin was correlated with serum IS levels in vivo. The same relationship was also observed in CRF rats with the continued administration of IS. In addition, IS dramatically increased the generation of ROS in both a dose-and time-dependent manner in HUVEC, suggesting that accumulated IS may play an important role in enhancing intravascular oxidative stress. Conclusion. We propose that AST-120 reduces IS concentrations in the blood that induces ROS production in endothelial cells, thereby inhibiting the subsequent occurrence of oxidative stress in the systemic circulation in renal failure.

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“…Oxidative stress is associated with accelerated plaque progression and increased CHD risk [13]. ROS are mainly produced by monocyte derived cells, smooth muscle and endothelial cells in the arterial wall in response to hypercholesterolemia and inflammatory mediators.…”

Section: Oxidative Stressmentioning

confidence: 99%