Inflammation, High Density Lipoprotein and Endothelium

ISSN: 1875-533X (Online)
ISSN: 0929-8673 (Print)

Volume 22, 38 Issues, 2015

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Atta-ur-Rahman, FRS
Honorary Life Fellow
Kings College
University of Cambridge

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Inflammation, High Density Lipoprotein and Endothelium

Author(s): Sepideh Madahian, Kaveh Daniel Navab, Nasim Pourtabatabaei, Seyedehsara Seyedali, Sheila Safar, Samra Vazirian and Greg Hough

Affiliation: David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.


High density lipoprotein (HDL) has two important roles: a) it modulates inflammation, and, b) it promotes reverse cholesterol transport. HDL cholesterol levels are inversely correlated with the risk of cardiovascular events. The main component of HDL, apolipoprotein A I (apo A I), is largely responsible for reverse cholesterol transport through the macrophage ATP binding cassette transporter ABCA1. Apo A I can be damaged by oxidative mechanisms, which render the protein less able to promote cholesterol efflux. HDL also contains a number of other proteins that are affected by the oxidative environment of the acute phase response. Modification of the protein components of HDL can convert it from an anti inflammatory to a pro inflammatory and dysfunctional particle. Small peptides that mimic some of the properties of apo A I have been shown in preclinical models to improve HDL function and reduce atherosclerosis without altering HDL cholesterol levels. Endothelium is the interface between the blood and the extra vascular environment regulating the traffic of vital molecules between the blood and tissues. Oxidative stress and excess levels of reactive oxygen species disrupt the normal function of endothelium. HDL and other antioxidant/anti-inflammatory systems prevent endothelial dysfunction and maintain the critical balance needed for normal vascular function.

Keywords: Endothelium, HDL, inflammation, Ox-lipids, PON1, ROS.

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Article Details

Volume: 21
Issue Number: 25
First Page: 2902
Last Page: 2909
Page Count: 8
DOI: 10.2174/0929867321666140414105530

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