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Activation of PPAR\u2010<jats:italic>\u03b3<\/jats:italic> has been shown to control the response of microglial cells, the main macrophage population found in brain parenchyma, and limit the inflammation. The anti\u2010inflammatory capacity of PPAR\u2010<jats:italic>\u03b3<\/jats:italic> agonists  has led to the hypothesis that PPAR\u2010<jats:italic>\u03b3<\/jats:italic> might be targeted to modulate  degenerative brain diseases in which inflammation has been increasingly recognized as a significant component. Recent experimental evidence suggests  that PPAR\u2010<jats:italic>\u03b3<\/jats:italic> agonists could be exploited to treat ocular diseases such as diabetic retinopathy, age\u2010related macular degeneration, autoimmune uveitis, and optic neuritis where inflammation  has relevant role. Additional  PPAR\u2010<jats:italic>\u03b3<\/jats:italic> agonist beneficial effects could involve amelioration of retinal microcirculation and inhibition of neovascularization. However,  PPAR\u2010<jats:italic>\u03b3<\/jats:italic> activation could, in some instances,  aggravate the ocular pathology, for example, by increasing the synthesis of vascular endothelial growth factor, a proangiogenic factor that could trigger a vicious circle and further deteriorate retinal perfusion. The development of new in vivo and in vitro models to study ocular inflammation and how to modulate for the eye benefit will be instrumental for the search of  effective therapies.<\/jats:p>","DOI":"10.1155\/2008\/295784","type":"journal-article","created":{"date-parts":[[2008,3,19]],"date-time":"2008-03-19T08:20:38Z","timestamp":1205914838000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["PPAR\u2010<i>\u03b3<\/i>, Microglial Cells, and Ocular Inflammation:  New Venues for Potential Therapeutic 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