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.

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

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

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.

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.

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

Chimeric RNAs are widely distributed spatiotemporally during human retinal development and have important regulatory functions, such as silencing of CTNNBIP1-CLSTN1 biasing the progenitor cells toward the RPE cell fate at the expense of neural retinal cell fates.

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.

Researchers have combined organ-on-a-chip engineering with the benefits of organoids to make improved models of the human retina.