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Dysfunctional HDL and atherosclerotic cardiovascular disease
Open accessAbstract
High-density lipoproteins (HDLs) protect against atherosclerosis by removing excess cholesterol from macrophages through the ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) pathways involved in reverse cholesterol transport. Factors that impair the availability of functional apolipoproteins or the activities of ABCA1 and ABCG1 could, therefore, strongly influence atherogenesis. HDL also inhibits lipid oxidation, restores endothelial function, exerts anti-inflammatory and antiapoptotic actions, and exerts anti-inflammatory actions in animal models. Such properties could contribute considerably to the capacity of HDL to inhibit atherosclerosis. Systemic and vascular inflammation has been proposed to convert HDL to a dysfunctional form that has impaired antiatherogenic effects. A loss of anti-inflammatory and antioxidative proteins, perhaps in combination with a gain of proinflammatory proteins, might be another important component in rendering HDL dysfunctional. The proinflammatory enzyme myeloperoxidase induces both oxidative modification and nitrosylation of specific residues on plasma and arterial apolipoprotein A-I to render HDL dysfunctional, which results in impaired ABCA1 macrophage transport, the activation of inflammatory pathways, and an increased risk of coronary artery disease. Understanding the features of dysfunctional HDL or apolipoprotein A-I in clinical practice might lead to new diagnostic and therapeutic approaches to atherosclerosis.
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“Some studies have indicated a complete loss of function and dysfunction gain concerning anti-inflammatory, vasodilatory, and antiapoptotic activities.”
From Residual Cardiovascular Risk: Role of Remnants Cholesterol, Monocyte/HDL Ratio and Lipoprotein Ratios on Personalized Cardiovascular Prevention (2024) · cites this paper as [9]
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“However, there are instances where HDL’s ability to deliver cholesterol esters via SCARB1 may be reduced, indicating only a partial loss of function.”
From Residual Cardiovascular Risk: Role of Remnants Cholesterol, Monocyte/HDL Ratio and Lipoprotein Ratios on Personalized Cardiovascular Prevention (2024) · cites this paper as [9]
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“It was noted that HDL could lose its anti-inflammatory properties and even develop proinflammatory characteristics.”
From Residual Cardiovascular Risk: Role of Remnants Cholesterol, Monocyte/HDL Ratio and Lipoprotein Ratios on Personalized Cardiovascular Prevention (2024) · cites this paper as [9]
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“However, when it comes to antioxidative activity and cholesterol efflux capacity, the deficiency observed in HDL’s normal function falls short of complete dysfunction [9].”
From Residual Cardiovascular Risk: Role of Remnants Cholesterol, Monocyte/HDL Ratio and Lipoprotein Ratios on Personalized Cardiovascular Prevention (2024) · cites this paper as [9]
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“Subsequent research has shown that the extent of HDL’s normal function loss and dysfunction gain can vary depending on its different biological activities.”
From Residual Cardiovascular Risk: Role of Remnants Cholesterol, Monocyte/HDL Ratio and Lipoprotein Ratios on Personalized Cardiovascular Prevention (2024) · cites this paper as [9]
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“Dysfunctional HDL (dys-HDL) are HDL cholesterol particles with high pro-atherogenic characteristics, characterized by the loss of typical antioxidant properties, becoming carriers of oxidized lipids themselves.”
From Residual Cardiovascular Risk: Role of Remnants Cholesterol, Monocyte/HDL Ratio and Lipoprotein Ratios on Personalized Cardiovascular Prevention (2024) · cites this paper as [9]
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“Moreover, modulations in HDL particle composition can transform it to dysfunctional and, through this modulation, increase the risk of CVD40.”
From Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses (2016) · cites this paper as [40]
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“Decrease in HDL has been regarded as one important risk factor for cardiovascular diseases40.”
From Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses (2016) · cites this paper as [40]
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Metadata
- Authors
- Rosenson, R. S., Brewer, H. B., Ansell, B. J., Barter, P., Chapman, M. J., Heinecke, J. W., Kontush, A., Tall, A. R., & Webb, N. R.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- MedStar Washington Hospital Center (US)
- University of California, Los Angeles (US)
- UNSW Sydney (AU)
- Inserm (FR)
- University of Washington (US)
- Columbia University (US)
- University of Kentucky (US)
- Corresponding author
- Rosenson, Robert S.
- Venue
- Nature Reviews Cardiology
- Published
- 2015-09-01
- Volume
- 13
- Issue
- 1
- Pages
- 48-60
- ISSN
- 1759-5002 (ISSN-L)
- 1759-5010
- PMC
- PMC6245940
- OpenAlex
- W2175680864
- Cited by
- 822
- References
- 131
- Citations by year
- 2026: 89 · 2025: 89 · 2024: 66 · 2023: 79 · 2022: 86 · 2021: 79 · 2020: 79 · 2019: 62 · 2018: 69 · 2017: 61 · 2016: 56 · 2015: 5
- FWCI
- 12.01
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DP3DK108209, P30DK017047)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Keywords
- HDL dysfunction, atherosclerosis, apolipoprotein A-I, reverse cholesterol transport, ABCA1, ABCG1, myeloperoxidase, nitrosylation, oxidative modification, inflammation, endothelial function, coronary artery disease, atherogenesis, anti-inflammatory activity
- MeSH terms
- Humans, Lipoproteins, HDL, Macrophages, Smoking, Apolipoprotein A-I, ATP-Binding Cassette Transporters, Diabetes Complications, Atherosclerosis, ATP Binding Cassette Transporter 1
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