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Review highlights the role of store-operated Ca2+ entry in retinal neurodegeneration, suggesting Ca2+ pathway targeting may improve glaucoma outcomes.
Ca 2+ homeostasis is essential for glial cell activity and normal neuronal function, and store-operated Ca 2+ entry (SOCE) is one mechanism that maintains it. The present review discusses the interplay between Ca 2+ dysregulation and microglial activation in glaucomatous retinal degeneration. We examine the impact of Ca 2+ homeostasis and SOCE on microglial function and their potential role in retinal ganglion cell degeneration and present the hypothesis that SOCE dysregulation may underlie glaucomatous pathology. This review suggests that targeting Ca 2+ pathways in microglial cells can be a potential treatment for glaucoma.
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Sofiia Baranykova (2025) studied this question.
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