PPAR-gamma: Difference between revisions

PPARγ is found in high levels in colonic epithelial cells.  The role of PPARγ in these cells may be related to regulation of immune response and colon inflammation [12].  The onset of Inflammatory Bowel Disease is thought to be caused by inflammatory cytokines present in the colon [12].  In patients with ulcerative colitis, colonic epithelial cells displayed impaired expression of PPARγ, an important mediator of aminosalicylate activities in Inflammatory Bowel Diseases [13].  TZD ligands could be implemented to reduce colonic inflammation [12].  Agonists have also been used in the treatment of colitis and psoriasis by inhibiting the inflammatory response of the epithelium and reducing cytokine production [8].  PPARγ inhibits activity of nuclear factor NFκB, which is higher in active ulcerative colitis patients [15].   

PPARγ could also be implemented in the treatment of other chronic inflammation-related diseases. Immunomodulatory effects have been found with PPARγ agonists [16].  Rosiglitazone alongside adiponectin reduces renal disease, atherosclerosis, and production of autoantibodies, all of which are characteristic of the inflammatory autoimmune disease Systemic Lupus Erythematosus (SLE) [16].  PPARγ ligands hold potential as cancer treatments [11] due to their ability to inhibit angiogenesis, the process required for the growth and metastasis of solid tumors [8]. PPARγ activators have pro-differentiation and anti-proliferation effects [3].  TZDs have also been shown to inhibit proliferation of human breast, prostate, and colon cancer cells [8].   

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