Key result
PAFR antagonists reduced oxLDL uptake and reversed oxLDL-induced CD36 expression in human monocytes/macrophages, suggesting oxLDL interacts with PAFR to increase CD36 expression.
oxLDL interacts with PAFR in macrophages to increase CD36 expression and oxLDL uptake, highlighting PAFR as a potential therapeutic target in atherosclerosis.
No takes yet. Share an insight, caveat, or question.
PAFR may be a target to limit macrophage oxLDL uptake; hypothesis-generating in vitro result leaves open in vivo and clinical validation.
Rios et al. (2011) studied Atherosclerosis. PAFR-antagonists (WEB2170, CV3988) vs. Diluents / Wild type was evaluated on Uptake of FITC-oxLDL and expression of CD36. PAFR antagonists reduced oxLDL uptake and reversed oxLDL-induced CD36 expression in human monocytes/macrophages, suggesting oxLDL interacts with PAFR to increase CD36 expression.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: