![]() This unique architecture provides exquisite sensitivity to changes in the retinal environment and allows MG to maintain retinal homeostasis and provide neural protection ( Vecino et al., 2016). They are radially oriented, extend the entire thickness of the tissue, and exhibit elaborate lateral processes contacting neighboring neurons. MG are the major glial cell type in the retina. Precedent for endogenous retinal repair has been clearly established for other vertebrate species, such as the zebrafish, which undergoes retinal regeneration fueled by a population of cells known as Müller glia (MG) ( Fausett and Goldman, 2006). ![]() Moreover, although progress has been made on all these fronts, this has not yet translated into a broad-spectrum clinical intervention to cure blindness.Īn alternative strategy seeks to determine whether the mammalian retina contains endogenous, but dormant, regenerative potential that might be awakened to drive tissue self-repair. However, it has become clear that a ‘one-size-fits-all’ approach to retinal repair is not likely to succeed, and treatments will have to be tailored to a variety of disease contexts, including stage of severity and affected cell type. Current approaches include delivery of trophic and anti-apoptotic factors, viral-mediated gene replacement therapy, transplantation of photoreceptors (rods and cones) and retinal pigment epithelium, optogenetic prosthesis, and bionic retinal implants ( Cepko, 2012 Fine et al., 2015 Langhe and Pearson, 2019). Owing to the clinical need for sight restoration, researchers are pursuing a variety of therapeutic strategies to delay or reverse retinal damage and neuronal death. Retinal degenerative diseases, as well as traumatic retinal injury, result in permanent loss of retinal neurons and thus sight, depriving many worldwide of one of our most valued senses. Here, we provide a summary of these emerging data and a discussion of technical concerns specific to AAV-mediated reprogramming experiments that must be addressed in order for the field to move forward. However, as researchers delve deeper into the cellular and molecular mechanisms, and further refine MG reprogramming strategies, we should recall past misinterpretations of data in this field and proceed with caution. The recent discovery that the Hippo signaling pathway acts as an intrinsic block to mammalian MG proliferation, along with reports of adeno-associated virus (AAV)-based MG reprogramming and functional photoreceptor differentiation, may indicate a watershed moment in the field of mammalian retinal regeneration. However, if we could understand the reasons why, we may be able to devise strategies to confer regenerative potential. Unfortunately, mammalian MG do not possess this ability. However, the MG of some non-mammalian species have the additional ability to generate new retinal neurons capable of sight restoration. As with all glial cells, the major role of retinal Müller glia (MG) is to provide essential neuronal support.
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