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Mouse models in which hypoxia can be genetically triggered in retinal pigmented epithelial cells show that hypoxia-induced metabolic stress alone can lead to photoreceptor atrophy/dysfunction.

Skin cells from a patient with retinitis pigmentosa have been used to generate induced pluripotent stem cells, which could potentially form the basis of new treatments for this disease.

NMNAT1, a ubiquitously expressed metabolic enzyme linked to inherited blinding disease, is crucial for the proper differentiation of photoreceptor cells and subsequent survival of multiple cell types in the retina.

Retinoic acid signaling from Muller glia is necessary for cone photoreceptor survival in the peripheral retina and is sufficient to promote cone survival in the central retina during retinal degeneration.

The retinoid-binding protein RLBP1 in the retinal pigment epithelium is crucially involved in cone photoreceptor visual pigment recycling and mimics the human eye disease with retinal lipid deposits when mutated.

High-throughput screening of over 6000 drugs using cells and retina tissue with a CEP290 ciliopathy mutation identified a small molecule, reserpine, which enhanced photoreceptor survival in retinal organoids and in a mouse disease model by partially restoring balance in proteostasis.

Müller glia cells in the medaka (Oryzias latipes) retina act as lineage restricted progenitors which only regenerate photoreceptors but can be activated to perform as potent stem cells using Sox2.

A neuroprotective role mediated by Strip1 maintains retinal ganglion cells during development, which ensures proper positioning of inner retinal neurons and preserves the laminar architecture of the inner retina.

Current understanding of Mertk biology, such as in retinal degeneration and tumor immunity, is redefined by gene knockout in C57BL/6 mice.

The retina compensates for rod death and deteriorating cones to retain high-fidelity visual signaling to the brain.