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.
3D niche topology imposes a spatially biased random stem cell loss, which is differentially fine-tuned in neural retina and retinal pigmented epithelium to regulate growth, shape, and cellular topology.
A microphysiological system (retina-on-a-chip) shows the potential to promote drug development and provide new insights into the underlying pathology of retinal diseases.
Metabolic relationships between cells in the retina and retinal pigment epithelium are fundamental to retinal function, retinal disease and age-related vision loss and they may provide strategies for metabolism-based therapies.
A new eye-specific Dcc mutant combined with an improved clearing protocol for the eye and brain (EyeDISCO) reveals the requirement of the receptor Dcc for retinal development and maintenance.
The protein p53 negatively impacts the ability of a CRISPR screen to discriminate between essential and non-essential genes, hence, p53 status should be considered in these screens.
The lens-averted domains of the optic vesicle are reservoirs of neuroretinal cells that flow into the developing optic cup in a process that is critically influenced by BMP signaling.
Vascular degeneration of the choroid and RPE disorganization were associated with pharmacological macrophage ablation, indicating that insufficiency of macrophage function may be a mechanism underlying age- and AMD-associated pathology.
Lipid efflux by the retinal pigment epithelium is crucial for proper retinal integrity and function, and its impairment may contribute to diseases like age-related macular degeneration.
