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Endothelial permeability, LDL deposition, and cardiovascular risk factors—a review
Open accessAbstract
Early atherosclerosis features functional and structural changes in the endothelial barrier function that affect the traffic of molecules and solutes between the vessel lumen and the vascular wall. Such changes are mechanistically related to the development of atherosclerosis. Proatherogenic stimuli and cardiovascular risk factors, such as dyslipidaemias, diabetes, obesity, and smoking, all increase endothelial permeability sharing a common signalling denominator: an imbalance in the production/disposal of reactive oxygen species (ROS), broadly termed oxidative stress. Mostly as a consequence of the activation of enzymatic systems leading to ROS overproduction, proatherogenic factors lead to a pro-inflammatory status that translates in changes in gene expression and functional rearrangements, including changes in the transendothelial transport of molecules, leading to the deposition of low-density lipoproteins (LDL) and the subsequent infiltration of circulating leucocytes in the intima. In this review, we focus on such early changes in atherogenesis and on the concept that proatherogenic stimuli and risk factors for cardiovascular disease, by altering the endothelial barrier properties, co-ordinately trigger the accumulation of LDL in the intima and ultimately plaque formation.
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“Cigarette smoke contributes to the progression of PAD by increasing endothelial cell permeability through formation of reactive oxygen species and enhancing inflammation, thus accelerating atherosclerosis within vessel walls.60”
From Racial and Ethnic Disparities in Peripheral Artery Disease (2021) · cites this paper as [60]
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Metadata
- Authors
- Mundi, S., Massaro, M., Scoditti, E., Carluccio, M. A., van Hinsbergh, V. W. M., Iruela-Arispe, M. L., & De Caterina, R.
- Affiliations
- University of Salento (IT)
- National Research Council (IT)
- Department of Physiology, Institute for Cardiovascular Research, VU University Medical Center, van der Boechorststraat, Amsterdam, The Netherlands
- Department of Molecular, Cell and Developmental Biology and Molecular Biology Institute, University of California, 610 Charles E Young Dr S, Los Angeles, USA; and
- Department of Neuroscience, Imaging and Clinical Science and Institute of Advanced Biomedical Technologies, University G. D'Annunzio, via dei Vestini, Chieti, Italy
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2017-12-08
- Volume
- 114
- Issue
- 1
- Pages
- 35-52
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- PMC
- PMC7729208
- OpenAlex
- W2772260227
- Semantic Scholar
- fc5863769c92f4f49350a944e5226d649a75f7ea
- Cited by
- 367
- References
- 266
- Citations by year
- 2026: 47 · 2025: 51 · 2024: 46 · 2023: 52 · 2022: 43 · 2021: 56 · 2020: 45 · 2019: 19 · 2018: 8
- FWCI
- 2.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- NIH
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- endothelial permeability, endothelial barrier function, atherosclerosis, cardiovascular risk factors, oxidative stress, reactive oxygen species, inflammation, dyslipidemia, diabetes mellitus, obesity, smoking, leukocyte infiltration, plaque formation, transendothelial transport
- MeSH terms
- Animals, Arteries, Biological Transport, Endothelium, Vascular, Humans, Lipoproteins, LDL, Permeability, Prognosis, Risk Factors, Smoking, Signal Transduction, Comorbidity, Reactive Oxygen Species, Oxidative Stress, Inflammation Mediators, Atherosclerosis, Plaque, Atherosclerotic
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 ›
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