By Jim W. Burgess, Philip A. Sinclair, Christophe M. Chretien, Jonathon Boucher (auth.), Associate Professor Sukhinder Kaur Cheema (eds.)

About the Series:

Advances in Biochemistry in Heath and Disease offers state of the art discussions in state of the art biochemical examine, supplying interesting advancements that impression healthcare and illness examine. Volumes within the sequence specialize in cross-disciplinary biomedical study and look at numerous issues in biochemistry, mobilephone biology, molecular biology, and biomedicine.

Biochemistry of Atherosclerosis

Sukhinder Kaur Cheema

Biochemistry of Atherosclerosis examines atherosclerosis in nice aspect, concentrating on the chance of atherosclerosis, and the biochemical pathways concerned. It offers a breadth of information in addition to new insights right into a number of themes in relation to atherosclerosis from best scientists all over the world who're on the vanguard of atherosclerosis study. Biochemistry of Atherosclerosis is vital interpreting for biomedical and medical researchers.

Key topics:

    • Hyperlipidaemia and Atherosclerosis
    • Diabetes brought on Atherosclerosis
    • Hypertension brought about Atherosclerosis
    • Homocysteine Metabolism and Atherosclerosis
    • Role of the Immune method in Atherosclerosis
    • Role of Infectious brokers in Atherogenesis
    • Dietary administration of Aherosclerosis

About the Editor:

Sukhinder Kaur Cheema is at present affiliate Professor of Biochemistry and a CIHR (Canadian Institutes of health and wellbeing study) New Investigator on the Memorial collage of Newfoundland. a professional in dietary biochemistry, lipid metabolism and heart problems, she is go appointed in college of medication on the Memorial collage of Newfoundland.

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Extra info for Biochemistry of Atherosclerosis

Sample text

Williams KJ, Fless GM, Petrie KA, Snyder ML, Brocia RW, Swenson TL: Mechanisms by which lipoprotein lipase alters cellular metabolism of lipoprotein(a), low density lipoprotein, and nascent lipoproteins. Roles for low density lipoprotein receptors and heparan sulfate proteoglycans. J Biol Chem 267: 13284–13292, 1992. 53. Rhainds D, Brissette L: Low density lipoprotein uptake: holoparticle and cholesteryl ester selective uptake. Int J Biochem Cell Biol 31: 915–931, 1999. 54. Wang N, Weng W, Breslow JL, Tall AR: Scavenger receptor BI (SR-BI) is upregulated in adrenal gland in apolipoprotein A-I and hepatic lipase knock-out mice as a response to depletion of cholesterol stores.

J Biol Chem 264: 21573–21581, 1989. Chapter 2. The Role of LCAT in Atherosclerosis 35 5. Lacko AG, Pritchard PH: International Symposium on Reverse Cholesterol Transport. Report on a meeting. J Lipid Res 31: 2295–2299, 1990. 6. Rader DJ: Regulation of reverse cholesterol transport and clinical implications. Am J Cardiol 92(4A): 42J–49J, 2003. 7. Knight BL: ATP-binding cassette transporter A1: regulation of cholesterol efflux. Biochem Soc Trans 32(Pt 1): 124–127, 2004. 8. Zhang Y, Zanotti I, Reilly MP, Glick JM, Rothblat GH, Rader DJ: Overexpression of apolipoprotein A-I promotes reverse transport of cholesterol from macrophages to feces in vivo.

Clinically, despite the disruption of the RCT pathway and the severe low level of HDL-C, CLD subjects are paradoxically not particularly predisposed to premature CHD [10, 16–18]. Instead, there is a high prevalence of glomerulopathy in these subjects [19]. Other phenotypes include modest hypertriglyceridemia (HTG), presence of LpX vesicles and mild anemia [20]. In FED, LCAT activity is absent selectively in the HDL fractions. In these subjects, HDL-C is markedly reduced but cholesterol esterification in the apoB-containing lipoprotein particles is relatively preserved.

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