Targeting Nuclear Hormone Receptors: PPARα Agonists as Potential Disease-Modifying Drugs for Rheumatoid Arthritis

Figure 2

A hypothetical model for PPARα-induced anti-inflammatory effects in rheumatoid arthritis. PPARα might suppress transcriptional activity of NFκB by several mechanisms: directly, by inducing IκB transcription or by inhibition of NFκB migration into nucleus. Another transcription factor AP-1 is also suppressed by PPARα. Down regulation of NFκB and AP-1 results in reduced synthesis of various mediators involved in joint inflammation and damage as well as in atherosclerotic plaque formation. NFκB: nuclear factor κB, IκB: inhibitor of κB, AP-1: activator protein 1.