MINI REVIEW article
Front. Aging Neurosci.
Sec. Neuroinflammation and Neuropathy
Volume 17 - 2025 | doi: 10.3389/fnagi.2025.1657590
Role of store-operated Ca2+ entry and STIM2 in retinal neurodegeneration during glaucoma
Provisionally accepted
- Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology in Warsaw (IIMCB), Warsaw, Poland
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Ca2+ homeostasis is essential for glial cell activity and normal neuronal function, and store-operated Ca2+ entry (SOCE) is one mechanism that maintains it. The present review discusses the interplay between Ca2+ dysregulation and microglial activation in glaucomatous retinal degeneration. We examine the impact of Ca2+ 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 Ca2+ pathways in microglial cells can be a potential treatment for glaucoma.
Keywords: Microglia, calcium homeostasis, STIM2, SOCE, Glaucoma, Retina, Retinal Ganglion Cells
Received: 01 Jul 2025; Accepted: 11 Sep 2025.
Copyright: © 2025 Baranykova. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Sofiia Baranykova, sofiabaranykova@gmail.com
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.