Revised: December 22, 2011
Accepted: January 2, 2012
Published online: April 9, 2012
Retinal ischemia is a common clinical entity and, due to relatively ineffective treatment, remains a common cause of visual impairment and blindness. Generally, ischemic syndromes are initially characterized by low homeostatic responses which, with time, induce injury to the tissue due to cell loss by apoptosis. In this respect, retinal ischemia is a primary cause of neuronal death. It can be considered as a sort of final common pathway in retinal diseases and results in irreversible morphological and functional changes. This review summarizes the recent knowledge on the effects of ischemia in retinal tissue and points out experimental strategies/models performed to gain better comprehension of retinal ischemia diseases. In particular, the nature of the mechanisms leading to neuronal damage (i.e., excess of glutamate release, oxidative stress and inflammation) will be outlined as well as the potential and most intriguing retinoprotective approaches and the possible therapeutic use of naturally occurring molecules such as neuropeptides. There is a general agreement that a better understanding of the fundamental pathophysiology of retinal ischemia will lead to better management and improved clinical outcome. In this respect, to contrast this pathological state, specific pharmacological strategies need to be developed aimed at the many putative cascades generated during ischemia.