Neural retina-derived retinoic acids synthesized by Aldh1a1 control choroidal vascular development by regulating RPE-secreted VEGF.

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.

Retinal pigment epithelium flattening is an efficient solution adopted by the fast-developing zebrafish to enable folding of the eye primordia, which contrasts with the proliferation-based mechanism used by amniotes.

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.

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.

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.

Robotic AI system automated discovery of optimum cell culture protocol, a most experience-dependent process in regenerative medicine.

Pigmentation that confers protective function of RPE is not underlaid by a specific gene expression profile, reviled by microscopic imaging together with single-cell RNA sequencing.

BalaT-dependent β-alanine trafficking pathway in retinal pigment cells is critical for maintaining synaptic transmission of photoreceptor neurons in Drosophila.

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.