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      Association between circulating oxidized low-density lipoprotein and atherosclerotic cardiovascular disease

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          Abstract

          Atherosclerosis is a chronic, progressive disease which eventually leads to coronary heart disease (CHD), ischemic stroke and other atherosclerotic cardiovascular disease (ASCVD). Numerous studies have demonstrated an atherogenic role of oxidized low-density lipoprotein (ox-LDL) in the progression of ASCVD. This article briefly reviews the atherogenic mechanism of ox-LDL, the methods of measuring ox-LDL in the circulation, effect of medical therapy and life-style modification on ox-LDL level, and the association between circulating ox-LDL and atherosclerosis, including clinical ASCVD events and subclinical atherosclerosis, in observational studies.

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          A receptor-mediated pathway for cholesterol homeostasis.

          M. Brown, J Goldstein (1986)
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            Scavenger receptors class A-I/II and CD36 are the principal receptors responsible for the uptake of modified low density lipoprotein leading to lipid loading in macrophages.

            Vidya Kunjathoor, Maria Febbraio, Eugene A. Podrez … (2002)
            Modification of low density lipoprotein (LDL) can result in the avid uptake of these lipoproteins via a family of macrophage transmembrane proteins referred to as scavenger receptors (SRs). The genetic inactivation of either of two SR family members, SR-A or CD36, has been shown previously to reduce oxidized LDL uptake in vitro and atherosclerotic lesions in mice. Several other SRs are reported to bind modified LDL, but their contribution to macrophage lipid accumulation is uncertain. We generated mice lacking both SR-A and CD36 to determine their combined impact on macrophage lipid uptake and to assess the contribution of other SRs to this process. We show that SR-A and CD36 account for 75-90% of degradation of LDL modified by acetylation or oxidation. Cholesteryl ester derived from modified lipoproteins fails to accumulate in macrophages taken from the double null mice, as assessed by histochemistry and gas chromatography-mass spectrometry. These results demonstrate that SR-A and CD36 are responsible for the preponderance of modified LDL uptake in macrophages and that other scavenger receptors do not compensate for their absence.
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              Modification of low density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low density lipoprotein phospholipids.

              John Leake, S S Parthasarathy, Urs P. Steinbrecher … (1984)
              Low density lipoprotein (LDL) incubated with cultured endothelial cells from rabbit aorta or human umbilical vein is altered in several ways (EC-modified): (i) It is degraded by macrophages much faster than LDL similarly incubated in the absence of cells or incubated with fibroblasts. (ii) Its electrophoretic mobility is increased. (iii) Its density is increased. We report here that antioxidants completely prevent these changes. We also report that these changes do not take place if transition metals in the medium are chelated with EDTA. During EC-modification as much as 40% of the LDL phosphatidylcholine is degraded to lysophosphatidylcholine by a phospholipase A2-like activity. When incubation conditions in the absence of cells were selected to favor oxidation--for example, by extending the time of incubation of LDL at low concentrations, or by increasing the Cu2+ concentration--LDL underwent changes very similar to those occurring in the presence of cells, including degradation of phosphatidylcholine. Hence, some phospholipase activity appears to be associated with the isolated LDL used in these studies. The results suggest a complex process in which endothelial cells modify LDL by mechanisms involving generation of free radicals and action of phospholipase (s).
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                Author and article information

                Contributors
                Jing Liu
                Journal
                Journal ID (nlm-ta): Chronic Dis Transl Med
                Journal ID (iso-abbrev): Chronic Dis Transl Med
                Title: Chronic Diseases and Translational Medicine
                Publisher: KeAi Publishing
                ISSN (Print): 2095-882X
                ISSN (Electronic): 2589-0514
                Publication date PMC-release: 25 May 2017
                Publication date Collection: 25 June 2017
                Publication date (Electronic): 25 May 2017
                Volume: 3
                Issue: 2
                Pages: 89-94
                Affiliations
                [1]Department of Epidemiology, Beijing An Zhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China
                Author notes
                [∗ ]Corresponding author. Tel.: +86 010 64456710. jingliu@ 123456ccmu.edu.cn
                Article
                Publisher ID: S2095-882X(16)30124-4
                DOI: 10.1016/j.cdtm.2017.02.008
                PMC ID: 5627698
                PubMed ID: 29063061
                SO-VID: 7c6d768e-4aae-42d7-bf2f-14f2b5c61547
                Copyright © © 2017 Chinese Medical Association. Production and hosting by Elsevier B.V. on behalf of KeAi Communications Co., Ltd.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 13 November 2016
                Categories
                Subject: Perspective

                Keywords: oxidized low density lipoprotein,atherosclerosis,cardiovascular disease,subclinical atherosclerosis,review
                Data availability:
                Keywords: oxidized low density lipoprotein, atherosclerosis, cardiovascular disease, subclinical atherosclerosis, review

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