The role of sulfur-containing amino acids in superoxide production and modification of low density lipoprotein by arterial smooth muscle cells.

Heinecke, Jay W.; Rosen, Henry; Suzuki, Lucy A.; Chait, Alan

doi:10.1016/s0021-9258(18)61082-8

Cited by 417 publications

(21 citation statements)

References 40 publications

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“…10,11 Oxidative stress in patients with CKD has been attributed to the effects of uremic toxins, angiotensin II, proinflammatory cytokines, and hyperhomocysteinemia. 12,13 Statins have been shown to reduce oxidative stress in hypercholesterolemic patients. 14,15 Vitamin E supplementation and homocysteine-lowering therapy have also been shown to reduce oxidative stress in several patient populations.…”

Section: P Atients With Mild To Moder-mentioning

confidence: 99%

Effect of a Treatment Strategy Consisting of Pravastatin, Vitamin E, and Homocysteine Lowering on Carotid Intima-Media Thickness, Endothelial Function, and Renal Function in Patients With Mild to Moderate Chronic Kidney Disease

Nanayakkara¹,

Guldener

Wee³

et al. 2007

Arch Intern Med

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Background: Patients with chronic kidney disease have an increased risk of cardiovascular disease. Oxidative stress has been proposed to play a role in the development of cardiovascular disease among these patients. Methods:We conducted a randomized, double-blind trial in 93 patients (Cockcroft-Gault equation: creatinine clearance, 38±15 [mean±SD] mL/min per 1.73 m 2 [0.63±0.25 mL/s per m 2 ]) to investigate the effect of a treatment strategy designed primarily to achieve stepwise oxidative stress reduction on common carotid intima-media thickness (CC-IMT), brachial artery flow-mediated dilatation (BA-FMD), albuminuria, and renal function. The treatment group received a regimen of pravastatin to which vitamin E supplementation was added after 6 months and homocysteine-lowering therapy after another 6 months. Blood pressure in both groups was managed according to a standard protocol. The placebo group received matching placebos. Measurement of CC-IMT and BA-FMD was performed at randomization after 6, 12, and 18 months. Patients were followed up for 2 years. Generalized estimating equations were used for analysis.Results: Compared with placebo, active treatment was associated with a decrease in CC-IMT (after 18 months: from 0.68 to 0.63 mm in the treatment group and from 0.65 to 0.71 mm in the placebo group; PϽ.001), an increase in BA-FMD (after 18 months: from 4.66% to 7.56% in the treatment group and from 6.21% to 4.73% in the placebo group; PϽ.001), and an attenuated increase in urinary albumin excretion over time (P=.04 for betweengroup difference after 24 months), but no effect was observed on renal function. Conclusion:In patients with mild to moderate chronic kidney disease, 18 months of a treatment strategy along with well-controlled blood pressure reduced CC-IMT and urinary albumin excretion and increased BA-FMD.

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Section: P Atients With Mild To Moder-mentioning

confidence: 99%

Effect of a Treatment Strategy Consisting of Pravastatin, Vitamin E, and Homocysteine Lowering on Carotid Intima-Media Thickness, Endothelial Function, and Renal Function in Patients With Mild to Moderate Chronic Kidney Disease

Nanayakkara¹,

Guldener

Wee³

et al. 2007

Arch Intern Med

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“…3,4 While other enzymatic defects can also produce homocystinuria, the observation 3 decades ago that vascular disease was common regardless of the source of the defect suggested that homocysteine may be responsible for the vascular abnormality. 5 Plausible mechanisms to mediate a deleterious effect of high homocysteine level include vascular endothelial dysfunction, [6][7][8][9] promotion of oxidation of lowdensity lipoprotein cholesterol, 10,11 vascular smooth cell proliferation, 12 and coagulation abnormalities. [13][14][15] Accumulating data from epidemiological studies suggested that individuals with even moderately elevated levels of homocysteine (eg, fasting blood levels exceeding approximately 16 µmol/L) have small to moderate increased risks of cardiovascular disease (CVD).…”

mentioning

confidence: 99%

Blood Levels of Homocysteine and Increased Risks of Cardiovascular Disease

Christen¹,

Ajani²,

Glynn³

et al. 2000

Arch Intern Med

284

164

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“…Effects on oxidant-antioxidant dynamics 89,90 are that homocysteine oxidizes LDL, promotes generation of free radicals; inhibits intracellular antioxidant enzymes; reduces bioavailability of NO; and activates poly-ADPribose polymerase, an important mediator of endothelial dysfunction.…”

Section: Mechanism Involved In the Atherothrombotic Effects Of Homocysteine 80mentioning

confidence: 99%

Atherosclerosis Pathophysiology and the Role of Novel Risk Factors: A Clinicobiochemical Perspective

Mallika

Goswami

Rajappa³

2007

Angiology

186

122

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Atherosclerosis is the root cause of the biggest killer of the 21st century. Mechanisms contributing to atherogenesis are multiple and complex. A number of theories-including the role of dyslipidemia, hypercoagulability, oxidative stress, endothelial dysfunction, and inflammation and infection by certain pathogens-have been propounded from time to time explain this complex phenomenon. Recently it has been suggested that atherosclerosis is a multifactorial, multistep disease that involves chronic inflammation at every step, from initiation to progression, and that all the risk factors contribute to pathogenesis by aggravating the underlying inflammatory process. A better understanding of the pathogenesis of atherosclerosis will aid in devising pharmaceutical and lifestyle modifications for reducing mortality resulting from coronary artery disease (CAD).A comprehensive literature search was conducted using the Web sites of the National Library of Medicine (http:// www.ncbl.nlm.nih.gov/) and PubMed Central, the US National Library of Medicine's digital archive of life sciences literature (http:// www.pubmedcentral.nih.gov/). The data were accessed from books and journals in which relevant articles in this field were published. The whole spectrum of coronary artery disease evolves through various events that lead to the formation and progression of atherosclerotic plaque and finally its complications. Atherosclerosis is the culprit behind coronary artery disease, cerebral vascular disease, and peripheral vascular disease. The pathogenic mechanisms are varied and complex. Of late, the role of lipoprotein (a), homocysteine, and inflammation and infection as prime culprits in pathogenesis of CAD is the subject of intense research and debate. The appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework to understand the clinical benefits of newer therapeutic strategies, and a better understanding of pathogenesis aids in formulating preventive and therapeutic strategies in reducing mortality resulting from CAD.An in-depth knowledge of the various pathogenic mechanisms involved in atherosclerosis can help in substantiating the current existing knowledge about the CAD epidemic. This knowledge will help clinicians to better manage the disease, which affects Indians in its most severe form.

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The role of sulfur-containing amino acids in superoxide production and modification of low density lipoprotein by arterial smooth muscle cells.

Cited by 417 publications

References 40 publications

Effect of a Treatment Strategy Consisting of Pravastatin, Vitamin E, and Homocysteine Lowering on Carotid Intima-Media Thickness, Endothelial Function, and Renal Function in Patients With Mild to Moderate Chronic Kidney Disease

Effect of a Treatment Strategy Consisting of Pravastatin, Vitamin E, and Homocysteine Lowering on Carotid Intima-Media Thickness, Endothelial Function, and Renal Function in Patients With Mild to Moderate Chronic Kidney Disease

Blood Levels of Homocysteine and Increased Risks of Cardiovascular Disease

Atherosclerosis Pathophysiology and the Role of Novel Risk Factors: A Clinicobiochemical Perspective

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