Journal
ATHEROSCLEROSIS
Volume 315, Issue -, Pages 111-125Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2020.09.020
Keywords
HDL; LDL; SR-BI; ALK-1; Caveolin; Transcytosis
Funding
- Canada Graduate Scholarship-Master's Award from the Canadian Institutes of Health Research
- Swiss National Science Foundation [31003A-160216, 310030_166391/1]
- Canada Research Chair in Mechanisms of Endothelial Permeability
- Canadian Institutes of Health Research [PJT-168947]
- Swiss National Science Foundation (SNF) [310030_166391] Funding Source: Swiss National Science Foundation (SNF)
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The accumulation of low-density lipoproteins (LDL) in the arterial wall plays a pivotal role in the initiation and pathogenesis of atherosclerosis. Conversely, the removal of cholesterol from the intima by cholesterol efflux to high density lipoproteins (HDL) and subsequent reverse cholesterol transport shall confer protection against atherosclerosis. To reach the subendothelial space, both LDL and HDL must cross the intact endothelium. Traditionally, this transit is explained by passive filtration. This dogma has been challenged by the identification of several rate-limiting factors namely scavenger receptor SR-BI, activin like kinase 1, and caveolin-1 for LDL as well as SR-BI, ATP binding cassette transporter G1, and endothelial lipase for HDL. In addition, estradiol, vascular endothelial growth factor, interleukins 6 and 17, purinergic signals, and sphingosine-1-phosphate were found to regulate transendothelial transport of either LDL or HDL. Thorough understanding of transendothelial lipoprotein transport is expected to elucidate new therapeutic targets for the treatment or prevention of atherosclerotic cardiovascular disease and the development of strategies for the local delivery of drugs or diagnostic tracers into diseased tissues including atherosclerotic lesions.
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