Transcriptional Repression of Atherogenic Inflammation: Modulation by PPARδ

See allHide authors and affiliations

Science  17 Oct 2003:
Vol. 302, Issue 5644, pp. 453-457
DOI: 10.1126/science.1087344

You are currently viewing the abstract.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

This article has a correction. Please see:


The formation of an atherosclerotic lesion is mediated by lipid-laden macrophages (foam cells), which also establish chronic inflammation associated with lesion progression. The peroxisome proliferator-activated receptor (PPAR) γ promotes lipid uptake and efflux in these atherogenic cells. In contrast, we found that the closely related receptor PPARδ controls the inflammatory status of the macrophage. Deletion of PPARδ from foam cells increased the availability of inflammatory suppressors, which in turn reduced atherosclerotic lesion area by more than 50%. We propose an unconventional ligand-dependent transcriptional pathway in which PPARδ controls an inflammatory switch through its association and disassociation with transcriptional repressors. PPARδ and its ligands may thus serve as therapeutic targets to attenuate inflammation and slow the progression of atherosclerosis.

    View Full Text

    Stay Connected to Science