Download Antioxidants and Cardiovascular Disease by Ulf Landmesser, Helmut Drexler (auth.), Martial G. Bourassa, PDF

By Ulf Landmesser, Helmut Drexler (auth.), Martial G. Bourassa, Jean-Claude Tardif (eds.)

ISBN-10: 0387295526

ISBN-13: 9780387295527

ISBN-10: 0387295534

ISBN-13: 9780387295534

Antioxidants and heart problems, moment variation addresses a posh yet very well timed and engaging challenge in cardiovascular medication. it truly is written by means of well-known specialists within the fields of atherosclerosis and antioxidants. it may be of curiosity not just to academicians but additionally to training physicians. the 1st 5 chapters evaluation the overall options of oxidative rigidity and their courting to lipid metabolism, endothelial disorder, genetics and transcriptional components. the following seven chapters describe lately outlined markers of oxidative rigidity, pharmacological compounds with antioxidant job, ordinary antioxidants present in micronutrients and in nutrient-rich diets, and reports the new proof for his or her efficacy or loss of efficacy in sufferers with heart problems or cardiovascular possibility components. The final seven chapters speak about the capability healing advantages of antioxidants in a couple of cardiovascular stipulations which come with atherosclerosis, restenosis after percutaneous coronary intervention, significant cardiovascular probability components similar to high blood pressure, diabetes mellitus and dyslipidemia, and left ventricular disorder and congestive middle failure.

Martial G. Bourassa, M.D. and Jean-Claude Tardif, M.D. are affiliated with the Montreal center Institute, learn heart and division of drugs, college of medication, collage of Montreal, Montreal, Quebec, Canada.

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For example, mice generated with SR-A deletion were found to be more susceptible to infections^^^^l Therefore, although atherosclerosis may be ameliorated, additional infectious and proliferative lesions may develop. Cholesterol homeostasis and foam cell formation Macrophages possess mechanisms for preserving intracellular cholesterol homeostasis via either ABCAl-mediated transport of unesterified cholesterol and phospholipids to nascent HDL and/or conversion of cholesterol to cholesteryl esters^^^'^^ These pathways appear to be overwhelmed in the setting of atherosclerosis through scavenger receptormediated uptake of modified lipoproteins resulting in foam cell formation {Figure 2).

66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 39 Simons LA, Reichl D, Myant NB et al. The metabolism of the apoprotein of plasma low density lipoprotein in familial hyperbetalipoproteinaemia in the homozygous form. Atherosclerosis 1975;21:283-98. Goldstein JL, Ho YK, Basu SK et al. Binding site on macrophages that mediates uptake and degradation of acetylated low density lipoprotein, producing massive cholesterol deposition. Proc Natl Acad Sci U S A 1979;76:333-7. Kodama T, Freeman M, Rohrer L et al.

SR-A and other oxLDL receptors (not downregulated) Macrophaga Figure 1. Mechanisms of OxLDL uptake by monocytes. Native LDL cannot induce foamcell formation because uptake is slow and because the LDL receptor downregulates. Either acetyl LDL or OxLDL can induce cholesterol accumulation in macrophages resulting in foam-cell formation because uptake is rapid and the scavenger receptors do not downregulate in response to an increase in cellular cholesterol. Reproduced with permission from Steinberg/^^ Further evidence for a potential clinically relevant mechanism of foam cell formation was provided by Steinberg and colleagues in 1981 when they showed that overnight incubation of LDL with a cultured monolayer of endothelial cells^^^\ vascular smooth muscle cells^^^^ or with peritoneal macrophages^'^^'^^^ in a medium rich in metal ions generated modified LDL with a marked increase in the rate of uptake and degradation by mouse peritoneal macrophages.

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Antioxidants and Cardiovascular Disease by Ulf Landmesser, Helmut Drexler (auth.), Martial G. Bourassa, Jean-Claude Tardif (eds.)

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