Molecular mechanisms of cell death in retina during development of age-related macular degeneration

Abstract

Age-related macular degeneration (AMD) is a chronic progressive disease characterized by damage to the central retina zone. Changes in choriocapillaries, retinal pigment epithelium (RPE), and Bruch’s membrane (typical for aging) underlie AMD pathogenesis; however, the mechanisms launching the transfer of typical age-related changes in the pathological process are unknown. The death of photoreceptors and irreversible loss of vision become the results of pathological changes in RPE and choroid. In spite of intensive studies of AMD pathogenesis, information on molecular genetic preconditions of the events leading to the death of photoreceptors (as well as about the pathways of their death) is extremely limited; this complicates the search for efficient methods of AMD treatment (first of all, the most widely spread atrophic (“dry”) form of the disease). Recent studies demonstrated that not only apoptotic but also autophagic and necrotic signaling cascades are involved in the cellular death of retinal cells. The published data on three main forms of the programmed cell death (apoptosis, necrosis, and autophagy) and their role in AMD pathogenesis are summarized in the present review.

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