The DOI matches its Crossref record; 147 of the 148 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Galis, Z. S., Sukhova, G. K., Lark, M. W., & Libby, P. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117619 · Cited by 2,537
The role of lipid peroxidation and antioxidants in oxidative modification of LDL
Esterbauer, H., Gebicki, J. M., Puhl, H., & Jürgens, G. (1992) · Free Radical Biology and Medicine · doi:10.1016/0891-5849(92)90181-f · Cited by 2,307
Ylä‐Herttuala, S., Palinski, W., Rosenfeld, M. E., Parthasarathy, S., Carew, T. E., Butler, S. S., Witztum, J. L., & Steinberg, D. H. (1989) · Journal of Clinical Investigation · doi:10.1172/jci114271 · Cited by 1,877
Low density lipoprotein undergoes oxidative modification in vivo.
Palinski, W., Rosenfeld, M. E., Ylä‐Herttuala, S., Gurtner, G. C., Socher, S. S., Butler, S. W., Parthasarathy, S., Carew, T. E., Steinberg, D. H., & Witztum, J. L. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.4.1372 · Cited by 1,514
The Response-to-Retention Hypothesis of Early Atherogenesis
Williams, K. J., & Tabas, I. (1995) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.15.5.551 · Cited by 1,413
Daugherty, A., Dunn, J. L., Rateri, D. L., & Heinecke, J. W. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117342 · Cited by 1,269
Extensive Nitration of Protein Tyrosines in Human Atherosclerosis Detected by Immunohistochemistry
Beckman, J. S., Ye, Y. Z., Anderson, P. G., Chen, J., Accavitti, M. A., Tarpey, M. M., & White, C. R. (1994) · Biological Chemistry Hoppe-Seyler · doi:10.1515/bchm3.1994.375.2.81 · Cited by 1,122
Glycosaminoglycans: molecular properties, protein interactions, and role in physiological processes
Jackson, R. L., Busch, S. J., & Cardin, A. D. (1991) · Physiological Reviews · doi:10.1152/physrev.1991.71.2.481 · Cited by 1,099
Lipoprotein lipase and lipolysis: central roles in lipoprotein metabolism and atherogenesis
Goldberg, I. J. (1996) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)37569-6 · Cited by 1,029
Hazen, S. L., & Heinecke, J. W. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119379 · Cited by 842
Research works printed but not linked: 2
- Borén, 1998, Engineering non-atherogenic low density lipoproteins: direct evidence for the “response-to-retention” hypothesis of atherosclerosis, Circulation, 98, I-314
- Hurt-Camejo, 1999, Inflammatory and atherogenic lipoprotein markers in patients with rheumatoid arthritis, Circulation, 100, I-813
Cited by
Sorted by citations
Tabas, I., Williams, K. J., & Borén, J. (2007) · Circulation · doi:10.1161/circulationaha.106.676890 · Cited by 1,399
Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities
Bäck, M., Yurdagul, A., Tabas, I., Öörni, K., & Kovanen, P. T. (2019) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0169-2 · Cited by 1,341
Self-citationHevonoja, T., Pentikäinen, M. O., Hyvönen, M., Kovanen, P. T., & Ala‐Korpela, M. (2000) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/s1388-1981(00)00123-2 · Cited by 439
Self-citationMonocyte recruitment and foam cell formation in atherosclerosis
Bobryshev, Y. V. (2005) · Micron · doi:10.1016/j.micron.2005.10.007 · Cited by 379
Nakashima, Y., Wight, T. N., & Sueishi, K. (2008) · Cardiovascular Research · doi:10.1093/cvr/cvn099 · Cited by 309
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
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
