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Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis820.40 kB
Published VersionCC BY V4.0, Open Access
Journal article
Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis
Frontiers in Cardiovascular Medicine, Vol.9, pp.1-11
2022
PMCID: PMC9199460
PMID: 35722128
Abstract
Atherosclerosis is an immuno-metabolic disease involving chronic inflammation, oxidative stress, epigenetics, and metabolic dysfunction. There is compelling evidence suggesting numerous modifications including the change of the size, density, and biochemical properties in the low-density lipoprotein (LDL) within the vascular wall. These modifications of LDL, in addition to LDL transcytosis and retention, contribute to the initiation, development and clinical consequences of atherosclerosis. Among different atherogenic modifications of LDL, oxidation represents a primary modification. A series of pathophysiological changes caused by oxidized LDL (oxLDL) enhance the formation of foam cells and atherosclerotic plaques. OxLDL also promotes the development of fatty streaks and atherogenesis through induction of endothelial dysfunction, formation of foam cells, monocyte chemotaxis, proliferation and migration of SMCs, and platelet activation, which culminate in plaque instability and ultimately rupture. This article provides a concise review of the formation of oxLDL, enzymes mediating LDL oxidation, and the receptors and pro-atherogenic signaling pathways of oxLDL in vascular cells. The review also explores how oxLDL functions in different stages of endothelial dysfunction and atherosclerosis. Future targeted pathways and therapies aiming at reducing LDL oxidation and/or lowering oxLDL levels and oxLDL-mediated pro-inflammatory responses are also discussed.
Details
- Title
- Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis
- Authors
- Hui Jiang (Author) - University of Science and Technology of ChinaYongwen Zhou (Author) - University of Science and Technology of ChinaSeyed M Nabavi (Author) - AMP Biotec SRL (Advanced Medical Pharma, BIOTEC) - Benevento, ItalyAmirhossein Sahebkar (Author) - Mashhad University of Medical SciencesPeter J Little (Author) - University of the Sunshine Coast, Queensland, School of Health and Behavioural Sciences - LegacySuowen Xu (Corresponding Author) - University of Science and Technology of ChinaJianping Weng (Corresponding Author) - University of Science and Technology of ChinaJianjun Ge (Corresponding Author) - University of Science and Technology of China
- Publication details
- Frontiers in Cardiovascular Medicine, Vol.9, pp.1-11
- Publisher
- Frontiers Research Foundation
- Date published
- 2022
- DOI
- 10.3389/fcvm.2022.925923
- ISSN
- 2297-055X
- PMID
- 35722128; PMC9199460
- Copyright note
- Copyright © 2022 Jiang, Zhou, Nabavi, Sahebkar, Little, Xu, Weng and Ge. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
- Organisation Unit
- School of Health; University of the Sunshine Coast, Queensland; School of Health and Behavioural Sciences - Legacy
- Language
- English
- Record Identifier
- 99649177502621
- Output Type
- Journal article
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