Endothelial permeability, LDL deposition, and cardiovascular risk factors—a review

Mundi, Santa; Massaro, Marika; Scoditti, Egeria; Carluccio, Maria Annunziata; van Hinsbergh, Victor W M; Iruela-Arispe, Marial Luisa; De Caterina, Raffaele

doi:10.1093/cvr/cvx226

Cited by 367Atherosclerosis and Cardiovascular DiseasesNitric Oxide and Endothelin EffectsBarrier Structure and Function Studies

Endothelial permeability, LDL deposition, and cardiovascular risk factors—a review

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Mundi, Santa, Massaro, Marika, Scoditti, Egeria, Carluccio, Maria Annunziata, van Hinsbergh, Victor W M, Iruela-Arispe, Marial Luisa, De Caterina, Raffaele·2018·Cardiovascular Research

DOI 10.1093/cvr/cvx226PMC PMC7729208

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Abstract

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.
“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]
Section 6.5 (Smoking; page not provided) links cigarette smoke to ROS production, increased endothelial permeability, and atherosclerosis across multiple vascular beds. The review supports the proposed mechanism, but it does not specifically establish progression of peripheral artery disease (PAD). (LLM, conf=0.85)
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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
ORCID: Massaro, Marika
Scoditti, Egeria
Carluccio, Maria Annunziata
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
DOI: 10.1093/cvr/cvx226
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 › 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

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Endothelial permeability, LDL deposition, and cardiovascular risk factors—a review

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