Transport of LDLs into the arterial wall: impact in atherosclerosis.
Level 5 - mechanism / opinion, no new human data
Narrative review describing biological mechanisms without systematic review methodology or new human clinical data.
PubMed 32773465 · doi:10.1097/MOL.0000000000000701
What was done
This narrative review summarizes recent published research regarding the molecular and cellular regulatory mechanisms of endothelial low-density lipoprotein (LDL) transcytosis and its contribution to the pathogenesis of atherosclerosis.
What was found
The abstract reports no quantitative data or numerical effect estimates. It qualitatively describes findings that caveolae, caveolin-1 (Cav-1), activin-like kinase 1 (ALK1), and scavenger receptor B1 (SR-B1) act as key mediators of endothelial LDL transport. Specifically, Cav-1 is required for caveolae formation and caveolae-mediated LDL uptake, whereas ALK1 and SR-B1 directly bind LDL to facilitate trans-endothelial passage.
Why it matters
Elucidating and targeting the molecular regulators of endothelial LDL transcytosis may provide therapeutic avenues to inhibit the earliest initiating events of atherosclerosis.
Limits
As a narrative review, the abstract provides no study selection criteria, sample sizes, or quantitative meta-analytic pooling. The reported findings reflect preclinical and mechanistic models without direct clinical trial evidence or quantification in human populations.
Cited by
- contradicts The endothelial spaces in the inner layer of the arterial wall are large enough for almost any size or shape of LDL particle to penetrate.