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
