Abstract
Recent studies have demonstrated that diabetic retinopathy has several characteristics of a chronic inflammatory disease, such as increased nitric oxide production, intracellular adhesion molecule-1 upregulation, leukostasis and increased vascular permeability. In addition, diabetes leads to the activation of caspase-1, the enzyme responsible for the production of the pro-inflammatory cytokines IL-1β and IL-18 in the retinae of diabetic animals and diabetic patients. Minocycline, a second-generation tetracycline derivative, was able to prevent the activation of capase-1 in the retinae of diabetic mice. Therefore, this review is focused on discussing the role of caspase-1 as a mediator of chronic inflammation and/or apoptosis inducer in the development of diabetic retinopathy and the suitability of caspase-1 as a new potential therapeutic target.