Potential roles of astrocytes and Muller cells in the pathogenesis of glaucoma

Glaucoma, a progressive optic neuropathy and the leading cause of blindness, is characterized by impairment or degeneration of retinal ganglion cells (RGCs), which transmit visual information to the brain. Currently, 70 million people worldwide are affected by glaucoma. Elevated intraocular pressure (LOP), a major risk factor of glaucoma, directly damages RGCs. However, a substantial proportion of glaucoma patients have a normal LOP level. In particular, over 90% of Japanese glaucoma patients are reported to have normal LOP levels. Thus, a new focus for glaucoma pathology has emerged. Glial cells contribute to tissue homeostasis. Under pathological conditions, glial cells become reactive, lose their homeostatic functions, and gain neurotoxic functions, which trigger neurodegeneration in several diseases including glaucoma. Reactive glial cells have been identified in the eyes of glaucoma patients. In a glaucoma animal model, reactive glial cells are observed at early stages of the disease when RGCs are intact, indicating the possible role of glial cells in the pathogenesis of glaucoma. In this review, we introduce potential roles of glial cells in the pathogenesis of glaucoma. We focus on the roles of the ocular macroglial cells such as astrocytes and Muller cells, and discuss their roles in the pathogenesis of glaucoma. (C) 2021 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.

Automated summary

Glaucoma, a progressive optic neuropathy and leading cause of blindness worldwide, is characterized by impairment of retinal ganglion cells (RGCs), with elevated intraocular pressure as a major risk factor. However, a notable proportion of patients, especially in Japan, have normal intraocular pressure. The role of glial cells in glaucoma pathogenesis is being increasingly recognized, with reactive glial cells identified in glaucoma patients and animal models, suggesting their potential involvement in the disease process.