Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 2019, 5743109

Cellular Signaling in Müller Glia: Progenitor Cells for Regenerative and Neuroprotective Responses in Pharmacological Models of Retinal Degeneration


Cellular Signaling in Müller Glia: Progenitor Cells for Regenerative and Neuroprotective Responses in Pharmacological Models of Retinal Degeneration

Yang Liu et al. J Ophthalmol.


Retinal degenerative diseases are a leading cause of visual impairment or blindness. There are many therapies for delaying the progression of vision loss but no curative strategies currently. Stimulating intrinsic neuronal regeneration is a potential approach to therapy in retinal degenerative diseases. In contrast to stem cells, as embryonic/pluripotent stem cell-derived retinal progenitor cell or mesenchymal stem cells, Müller glia provided an endogenous cellular source for regenerative therapy in the retina. Müller glia are a major component of the retina and considerable evidence suggested these cells can be induced to produce the lost neurons in several species. Understanding the specific characteristic of Müller glia to generate lost neurons will inspire an attractive and alternative therapeutic strategy for treating visual impairment with regenerative research. This review briefly provides the different signal transduction mechanisms which are underlying Müller cell-mediated neuroprotection and neuron regeneration and discusses recent advances about regeneration from Müller glia-derived progenitors.


Figure 1
Figure 1
Signaling pathways regulating Müller glia cell dedifferentiation and proliferation following retinal injury induced by NMDA: pro, proliferation; dedi, dedifferentiation; neuro, neuroprotective.

Similar articles

See all similar articles

Cited by 2 articles


    1. Medeiros F. A., Lisboa R., Weinreb R. N., Liebmann J. M., Girkin C., Zangwill L. M. Retinal ganglion cell count estimates associated with early development of visual field defects in glaucoma. Ophthalmology. 2013;120(4):736–744. doi: 10.1016/j.ophtha.2012.09.039. - DOI - PMC - PubMed
    1. Cideciyan A. V., Sudharsan R., Dufour V. L., et al. Mutation-independent rhodopsin gene therapy by knockdown and replacement with a single AAV vector. Proceedings of the National Academy of Sciences. 2018;115(36):E8547–E8556. doi: 10.1073/pnas.1805055115. - DOI - PMC - PubMed
    1. Jonas J. B. Global prevalence of age-related macular degeneration. The Lancet Global Health. 2014;2(2):e65–e66. doi: 10.1016/s2214-109x(13)70163-3. - DOI - PubMed
    1. Liu H., Tang J., Du Y., et al. Photoreceptor cells influence retinal vascular degeneration in mouse models of retinal degeneration and diabetes. Investigative Opthalmology and Visual Science. 2016;57(10):4272–4281. doi: 10.1167/iovs.16-19415. - DOI - PMC - PubMed
    1. Hahn J. S., Aizenman E., Lipton S. A. Central mammalian neurons normally resistant to glutamate toxicity are made sensitive by elevated extracellular Ca2+: toxicity is blocked by the N-methyl-D-aspartate antagonist MK-801. Proceedings of the National Academy of Sciences. 1988;85(17):6556–6560. doi: 10.1073/pnas.85.17.6556. - DOI - PMC - PubMed

LinkOut - more resources