Functionality of HDL: Antioxidation and Detoxifying Effects
Open accessAbstract
High-density lipoproteins (HDL) are complexes of multiple talents, some of which have only recently been recognised but all of which are under active investigation. Clinical interest initially arose from their amply demonstrated role in atherosclerotic disease with their consequent designation as a major cardiovascular disease (CVD) risk factor. However, interest is no longer confined to vascular tissues, with the reports of impacts of the lipoprotein on pancreatic, renal and nervous tissues, amongst other possible targets. The ever-widening scope of HDL talents also encompasses environmental hazards, including infectious agents and environmental toxins. In almost all cases, HDL would appear to have a beneficial impact on health. It raises the intriguing question of whether these various talents emanate from a basic ancestral function to protect the cell.The following chapter will illustrate and review our current understanding of some of the functions attributed to HDL. The first section will look at the antioxidative functions of HDL and possible mechanisms that are involved. The second section will focus specifically on paraoxonase-1 (PON1), which appears to bridge the divide between the two HDL functions discussed herein. This will lead into the final section dealing with HDL as a detoxifying agent protecting against exposure to environmental pathogens and other toxins.
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HDL can protect against atherosclerosis by multiple mechanisms, including the ability to efflux cholesterol from endothelial macrophages (macrophage reverse cholesterol transport), or through anti-inflammatory, antioxidative and antiapoptotic pathways.
“HDL can protect against atherosclerosis by multiple mechanisms, including the ability to efflux cholesterol from endothelial macrophages (macrophage reverse cholesterol transport)43, or through anti-inflammatory44, antioxidative45 and antiapoptotic46 pathways.”
From Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses (2016) · cites this paper as [45]
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Self-citation
Flagged first, then by citations
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Cited by
Sorted by citations
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- Authors
- Karlsson, H., Kontush, A., & James, R. W.
- Affiliations
- Inserm (FR)
- University of Geneva (CH)
- Corresponding author
- James, Richard W.
- Venue
- Handbook of Experimental Pharmacology
- Publisher
- Springer International Publishing
- Published
- 2014-12-01
- Volume
- 224
- Pages
- 207-228
- ISSN
- 0171-2004 (ISSN-L)
- 1865-0325
- OpenAlex
- W36419898
- Cited by
- 55
- References
- 119
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 3 · 2020: 6 · 2019: 7 · 2018: 6 · 2017: 6 · 2016: 7 · 2015: 3
- FWCI
- 5.63
- Type
- book chapter
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Handbook of experimental pharmacology (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- National Research Foundation
- Institut National de la Santé et de la Recherche Médicale
- Université de Genève
- Fondation Novartis Consumer Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Keywords
- high-density lipoprotein, antioxidant function, detoxification, paraoxonase 1, atherosclerosis, cardiovascular risk, environmental toxins, infectious agents, lipoprotein function, tissue protection
- MeSH terms
- Animals, Antioxidants, Environmental Exposure, Humans, Lipoproteins, HDL, Oxidative Stress, Aryldialkylphosphatase
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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