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Aggregation, fusion, and vesicle formation of modified low density lipoprotein particles: molecular mechanisms and effects on matrix interactions
Open accessAbstract
Initiation of atherosclerosis is characterized by accumulation of aggregates of small lipid droplets and vesicles in the extracellular matrix of the arterial intima. The droplets and vesicles have features that suggest that they are formed from modified plasma-derived low density lipoprotein (LDL) particles. A variety of hydrolytic enzymes and prooxidative agents that could lead to extracellular assembly of LDL-derived droplets and vesicles are present in the arterial intima. In fact, in vitro studies have demonstrated that extensive oxidation of LDL and treatment of LDL with either proteolytic or lipolytic enzymes will induce LDL aggregation and fusion and treatment of LDL with cholesterol esterase will cause formation of vesicles. Fusion of LDL particles proceeds faster in vitro when they are bound to components of the extracellular matrix derived from the arterial intima, such as proteoglycans, and, depending on the type of modification, the strength of binding of modified LDL to the matrix components may either increase or decrease. In the present article, we discuss molecular mechanisms that provide clues as to how aggregated lipid droplets and vesicles may be derived from modified LDL particles. We also describe how these modified forms of LDL, by means of their trapping to the extracellular matrix, may lead to extracellular lipid accumulation in the arterial intima.
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“The retained lipoproteins (that is, those bound to the extracellular matrix of the arterial intima) are susceptible to modification by intimal oxidizing agents, proteases and lipases43,46,47.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [46]
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“Oxidative, proteolytic and lipolytic modifications induce LDL aggregation46, and the aggregation susceptibility of LDL was shown to be associated with the risk of cardiovascular death55.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [46]
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Self-citation
Metadata
- Authors
- Öörni, K., Pentikäinen, M. O., Ala-Korpela, M., & Kovanen, P. T.
- Affiliations
- Wihuri Research Institute (FI)
- Corresponding author
- Kovanen, Petri T.
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 2000-11
- Volume
- 41
- Issue
- 11
- Pages
- 1703-1714
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W1853133898
- Cited by
- 252
- References
- 148
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 4 · 2023: 5 · 2022: 6 · 2021: 13 · 2020: 9 · 2019: 8 · 2018: 11 · 2017: 4 · 2016: 5 · 2015: 8 · 2014: 12 · 2013: 8 · 2012: 21
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Lipid Research (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Keywords
- modified low-density lipoprotein, LDL oxidation, lipoprotein aggregation, vesicle formation, lipid droplets, atherosclerosis initiation, extracellular matrix, proteoglycans, cholesterol esterase, lipolytic enzymes, proteolytic enzymes, arterial intima
- MeSH terms
- Animals, Arteries, Arteriosclerosis, Chemistry, Physical, Extracellular Matrix, Humans, Lipolysis, Lipoproteins, LDL, Liposomes, Endopeptidases, Proteoglycans, Chemical Phenomena
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