Foam cells in atherosclerosis.
Level 5 - mechanism / opinion, no new human data
Narrative review of cellular mechanisms without primary human data
PubMed 23782937 · doi:10.1016/j.cca.2013.06.006
What was done
This narrative review summarizes the cellular mechanisms regulating macrophage foam cell formation in atherosclerosis, focusing on the pathways of cholesterol uptake (mediated by CD36 and SR-A), intracellular esterification (regulated by ACAT1 and nCEH), and cholesterol efflux (mediated by ABCA1, ABCG1, and SR-BI).
What was found
The abstract reports no quantitative empirical data. It describes the mechanistic balance of macrophage lipid metabolism: increased cholesterol influx and esterification paired with decreased outflow drives the transformation of macrophages into lipid-laden foam cells within atherosclerotic plaques.
Why it matters
Clarifies the primary molecular transporters and enzymes controlling macrophage cholesterol homeostasis, highlighting potential therapeutic targets to prevent or reverse foam cell formation in atherosclerosis.
Limits
The abstract contains no primary experimental data, quantitative findings, or systematic literature search criteria. As a narrative overview of molecular mechanisms, it does not assess clinical efficacy or human patient outcomes.
Cited by
- contradicts HDL particles can penetrate the inner layer of the arterial wall, bind to LDL, absorb cholesterol and triglycerides, and transport them back to the liver.