IMR Press / FBL / Volume 27 / Issue 6 / DOI: 10.31083/j.fbl2706169
Open Access Review
Harnessing the Neuroprotective Behaviors of Müller Glia for Retinal Repair
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1 Department of Biomedical Engineering, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA
*Correspondence: (Maribel Vazquez)
Academic Editor: Graham Pawelec
Front. Biosci. (Landmark Ed) 2022, 27(6), 169;
Submitted: 20 January 2022 | Revised: 18 April 2022 | Accepted: 5 May 2022 | Published: 30 May 2022
(This article belongs to the Special Issue Recent Advances in Eye and Vision Research)
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Progressive and irreversible vision loss in mature and aging adults creates a health and economic burden, worldwide. Despite the advancements of many contemporary therapies to restore vision, few approaches have considered the innate benefits of gliosis, the endogenous processes of retinal repair that precede vision loss. Retinal gliosis is fundamentally driven by Müller glia (MG) and is characterized by three primary cellular mechanisms: hypertrophy, proliferation, and migration. In early stages of gliosis, these processes have neuroprotective potential to halt the progression of disease and encourage synaptic activity among neurons. Later stages, however, can lead to glial scarring, which is a hallmark of disease progression and blindness. As a result, the neuroprotective abilities of MG have remained incompletely explored and poorly integrated into current treatment regimens. Bioengineering studies of the intrinsic behaviors of MG hold promise to exploit glial reparative ability, while repressing neuro-disruptive MG responses. In particular, recent in vitro systems have become primary models to analyze individual gliotic processes and provide a stepping stone for in vivo strategies. This review highlights recent studies of MG gliosis seeking to harness MG neuroprotective ability for regeneration using contemporary biotechnologies. We emphasize the importance of studying gliosis as a reparative mechanism, rather than disregarding it as an unfortunate clinical prognosis in diseased retina.

Müller glia
in vitro
Fig. 1.
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