Macular edema is defined as an accumulation of fluid in the outer plexiform layer and the inner nuclear layer as well as a swelling of Müller cells of the retina. It consists of a localized expansion of the retinal extracellular space (sometimes associated with the intracellular space) in the macular area. Macular edema is a common cause of a sudden or chronic decrease in visual acuity occurring in many ocular diseases such as age-related macular degeneration, diabetic retinopathy and retinal vein occlusion. As a nonspecific sign of many intraocular and systemic diseases, macular edema represents a common final pathway. The existence of the blood-retinal barrier (BRB) formed by intercellular junctions is the precondition required to maintain this physiological status. This status may become severely disturbed by many diseases, finally resulting in macular edema. In this article, the development of macular edema will also be classified by its pathophysiological and pathobiochemical pathways. Vascular components, the dysfunctional BRB, the role of proteins and water fluxes as well as the role of several inflammatory mediators (e.g. angiotensin II, vascular endothelial growth factor, prostaglandins) in the retina will be discussed as responsible mechanisms leading to the development of macular edema.

It is now well-known that AMD is a multi-factorial disease, with environmental causes and genetics all playing a role.

Choroidal neovascularization (CNV) secondary to age-related macular degeneration (AMD) is now the leading cause of blindness and severe vision loss among people over the age of 40 in the Western world. Its prevalence is certain to increase substantially as the population ages. Treatments currently available for the disease include laser photocoagulation, verteporfin photodynamic therapy, and intravitreal injections of corticosteroids and anti-angiogenic agents. Many studies have reported the benefits of each of these treatments, although none is without its risks. No intervention actually cures AMD, nor the neovascularization associated with it. However, its symptoms are treated with varying degrees of success. Some treatments stabilize or arrest the progress of the disease. Others have been shown to reverse some of the damage that has already been done. These treatments can even lead to visual improvement. This paper will review the major classes of drugs and therapies designed to treat this condition.

Both diminution of angiostatic and increment of angiogenic factors seem to contribute to neovascularization in the eye under pathologic conditions. They are presented here separately. The involved proteins can change their role during the process of neovascularization from promoters to inhibitors and vice versa. Angiostatic factors can be divided into passive, active, unspecific and specific ones.Some of them act during neovascularization as members of feedback loops by modifying the effects of their angiogenic counterparts. Among the angiogenic factors VEGF is the most important.Nevertheless other stimulating proteins exist in large numbers. Together with their static counterparts they form a complex network which controls neovascularization under physiologic as well aspathologic conditions.