Abstract
Glaucoma is the second leading cause of blindness worldwide, affecting ~80 million people by 2020 (1, 2). The condition is characterized by a progressive loss of retinal ganglion cells (RGCs) and their axons accompanied by visual field loss. The underlying pathophysiology of glaucoma remains elusive. Glaucoma is recognized as a multifactorial disease, and lowering intraocular pressure (IOP) is the only treatment that has been shown to slow the progression of the condition. However, a significant number of glaucoma patients continue to go blind despite intraocular pressure-lowering treatment (2). Thus, the need for alternative treatment strategies is indisputable. Accumulating evidence suggests that glial cells play a significant role in supporting RGC function and that glial dysfunction may contribute to optic nerve disease. Here, we review recent advances in understanding the role of glial cells in the pathophysiology of glaucoma. A particular focus is on the dynamic and essential interactions between glial cells and RGCs and potential therapeutic approaches to glaucoma by targeting glial cells.
Highlights
Glaucoma is a group of eye diseases that can cause vision loss and blindness
The most investigated risk factors for glaucoma progression include intraocular pressure (IOP), age, genetic background, thinner corneal thickness, and vascular dysregulation [11], other disease mechanisms such as oxidative stress, mitochondrial dysfunction, excitotoxicity, and immunological processes may contribute to the pathophysiology of the disease [2, 12, 13]
Accumulating evidence suggests that both types of glial cells are interacting with the retinal and optic nerves, and are important contributors to the pathophysiological processes leading to glaucomatous retinal ganglion cells (RGCs) loss [14, 15, 17, 23, 32,33,34]
Summary
Glaucoma is a group of eye diseases that can cause vision loss and blindness. The number of people with glaucoma is increasing due to the age-related nature of the disease [3]. The most investigated risk factors for glaucoma progression include IOP, age, genetic background, thinner corneal thickness, and vascular dysregulation [11], other disease mechanisms such as oxidative stress, mitochondrial dysfunction, excitotoxicity, and immunological processes may contribute to the pathophysiology of the disease [2, 12, 13] In this context, accumulating evidence suggests that glial cells in the retina and optic nerve may play important roles in the pathogenesis of RGCs [14,15,16]. It is evident that the glial response to injury stimuli can further perpetuate RGC damage [17, 23, 25, 26] Despite these important advances in our understanding of the interactions between glia and retinal neurons in health and in the context of glaucoma, there is still much to be learned. Accumulating evidence suggests that both types of glial cells are interacting with the retinal and optic nerves, and are important contributors to the pathophysiological processes leading to glaucomatous RGC loss [14, 15, 17, 23, 32,33,34]
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