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Endothelial permeability, LDL deposition, and cardiovascular risk factors-a review
Santa Mundi1, Marika Massaro2, Egeria Scoditti2
1Department of Biological and Environmental Science and Technology (DISTEBA), University of Salento, via Monteroni, 73100, Lecce, Italy.
Insights
Cardiovascular risk factors increase endothelial permeability via oxidative stress, leading to low-density lipoprotein (LDL) deposition and plaque formation in early atherosclerosis.
Area of Science:
- Vascular Biology
- Cardiovascular Disease Pathophysiology
- Endothelial Function
Background:
- Early atherosclerosis involves endothelial barrier dysfunction, impacting molecular transport between blood and vessel walls.
- This dysfunction is mechanistically linked to atherosclerosis development.
- Proatherogenic stimuli and cardiovascular risk factors (dyslipidemias, diabetes, obesity, smoking) are key contributors.
Purpose of the Study:
- To review early changes in atherogenesis.
- To explore the role of endothelial barrier alterations in initiating atherosclerosis.
- To highlight the common signaling pathway involving oxidative stress.
Main Methods:
- Review of existing literature on endothelial barrier function in early atherosclerosis.
- Analysis of signaling pathways affected by proatherogenic stimuli.
- Focus on the interplay between endothelial permeability, oxidative stress, and lipoprotein accumulation.
Main Results:
- Proatherogenic stimuli increase endothelial permeability through oxidative stress (imbalanced reactive oxygen species production/disposal).
- This leads to a pro-inflammatory state, altering gene expression and endothelial transport.
- Increased permeability facilitates low-density lipoprotein (LDL) deposition and leukocyte infiltration.
Conclusions:
- Proatherogenic stimuli and cardiovascular risk factors disrupt endothelial barrier properties.
- This disruption is a coordinated trigger for LDL accumulation and subsequent plaque formation.
- Understanding these early endothelial changes is crucial for preventing atherosclerosis.
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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