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Autophagy in the eye: from physiology to pathophysiology

Paloma B. Liton, Kathleen Boesze-Battaglia, Michael E. Boulton, Patricia Boya, Thomas A. Ferguson, Ian G. Ganley, Anu Kauppinnen, Gordon W. Laurie, Noboru Mizushima, Hideaki Morishita,j, Rossella Russo, Jaya Sadda, Rajalekshmy Shyam, Debasish Sinha, Debra A. Thompson and David N. Zacks

Autophagy is a catabolic self-degradative pathway that promotes the degradation and recycling of intracellular material through the lysosomal compartment. Although first believed to function in conditions of nutritional stress, autophagy is emerging as a critical cellular pathway, involved in a variety of physiological and pathophysiological processes. Autophagy dysregulation is associated with an increasing number of diseases, including ocular diseases. On one hand, mutations in autophagy-related genes have been linked to cataracts, glaucoma, and corneal dystrophy; on the other hand, alterations in autophagy and lysosomal pathways are a common finding in essentially all diseases of the eye. Moreover, LC3-associated phagocytosis, a form of non-canonical autophagy, is critical in promoting visual cycle function. This review collects the latest understanding of autophagy in the context of the eye. We will review and discuss the respective roles of autophagy in the physiology and/or pathophysiology of each of the ocular tissues, its diurnal/circadian variation, as well as its involvement in diseases of the eye.

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