High Density Lipoproteins: From Biological Understanding to Clinical Exploitation (Handbook of Experimental Pharmacology)

High Density Lipoproteins: From Biological Understanding to Clinical Exploitation (Handbook of Experimental Pharmacology)

Language: English

Pages: 694

ISBN: 3319096648

Format: PDF / Kindle (mobi) / ePub

In this Handbook of Experimental Pharmacology on “High Density Lipoproteins – from biological understanding to clinical exploitation” contributing authors (members of COST Action BM0904/HDLnet) summarize in more than 20 chapters our current knowledge on the structure, function, metabolism and regulation of HDL in health and several diseases as well as the status of past and ongoing attempts of therapeutic exploitation.

The book is of interest to researchers in academia and industry focusing on lipoprotein metabolism, cardiovascular diseases and immunology as well as clinical pharmacologists, cardiologists, diabetologists, nephrologists and other clinicians interested in metabolic or inflammatory diseases.

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Primary Regulators of Plasma HDL Cholesterol For the de novo production of HDL, the small intestine and liver need to produce apolipoprotein (apo) A-I, ATP-binding cassette protein A1, and lecithin–cholesterol acyltransferase encoded by the APOAI, ABCA1, and LCAT genes, respectively. When the production of any of these proteins is attenuated (through functional large-impact mutations), it immediately translates into a reduction of HDL cholesterol in the circulation. Other established modulators

et al. 2013). Conclusion In addition to reverse transport of cholesterol, HDL particles display different protective effects that could support their use in the acute phase of stroke. Different neuroprotective drugs proven to be effective in animal models have failed to translate into clinical settings (Xu and Pan 2013). Early treatments that could be used without interfering with fibrinolytic treatments should be considered as a good option to limit the deleterious effects of ischaemic stroke.

reversed after smoking cessation (James et al. 2000). The mechanistic data for the effects of smoking on HDL function are far from comprehensive and merit further investigation. 4.3 Smoking Cessation Intervention to Increase Plasma HDL Concentration The majority of smoking cessation studies are small, and most, but not all, have been shown to result in a rise in HDL concentration. A meta-analysis of 27 studies incorporating over 6,000 subjects indicated that HDL-C increased by 0.10 mmol/L after

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Scott R, Kim JB, Xue A, Gebski V, Wasserman SM, Stein EA (2012) Effect of a monoclonal antibody to PCSK9 on low-density lipoprotein cholesterol levels in statin-intolerant patients: the GAUSS randomized trial. JAMA 308:2497–2506PubMed Sun D, Zhang J, Xie J, Wei W, Chen M, Zhao X (2012) MiR-26 controls LXR-dependent cholesterol efflux by targeting ABCA1 and ARL7. FEBS Lett 586:1472–1479PubMed Swayze EE, Siwkowski AM, Wancewicz EV, Migawa MT, Wyrzykiewicz TK, Hung G, Monia BP, Bennett CF (2007)

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