Table 1.
Growth factors, cytokines, chemokines, and other proinflammatory mediators downregulated by PPARγ activation. PDGF-BB, platelet-derived growth factor-BB homodimer; AP-1, activated protein-1; NF-κB = nuclear factor-κB; NFAT = nuclear factor of activated T lymphocytes; STAT = signal transducer and activator of transcription; ICAM, intracellular adhesion molecule; VCAM, vascular cell adhesion molecule; iNOS, inducible nitric oxide synthase. (Adapted with permission from: B. Staels, “PPARγ and atherosclerosis.” Current Medical Research and Opinion, vol. 21, Suppl. 1, pp. S13-S20, 2005; H. A. Pershadsingh, “Dual peroxisome proliferator-activated receptor-alpha/gamma agonists : in the treatment of type 2 diabetes mellitus and the metabolic syndrome.” Treatments in Endocrinology, vol. 5, no. 2, pp. 89-99, 2006.)
Growth factors | Cytokines | Chemokines | Nuclear transcription factors | Other molecules |
---|---|---|---|---|
ATII | IL-1β | IL-8 | AP-1 | IFN-γ |
TGF-β | IL-2 | MCP-1 | NF-κB | iNOS |
ET-1 | IL-6 | RANTES | STAT | PAI-1 |
bFGF | TNF-α | NFAT | MMP-2 | |
PDGF-BB | MMP-9 | |||
EGF | VCAM-1 | |||
VEGF | ICAM-1 | |||
E-selectin |