Unveiling the cellular and molecular mechanisms of diabetic retinopathy with human retinal organoids.

ABSTRACT: Diabetic retinopathy (DR) is a leading cause of vision impairment worldwide, driven by chronic hyperglycaemia and its complex metabolic consequences. While animal models have been widely used to study DR, they often fail to replicate the physiology of the human retina. Here, we employed human retinal organoids to investigate the effects of incremental hyperglycaemic stress-a modest increase from a standard high-glucose baseline (17.5 mM) to 25 mM D-glucose-across different stages of retinal differentiation. Early-stage organoids demonstrated resilience to high-glucose levels, maintaining normal morphology, viability, and gene expression. In contrast, late-stage organoids exhibited marked photoreceptor vulnerability, including downregulation of outer segment (OS)-specific genes, shortened O

SUBMITTER: Polesovska L 

PROVIDER: S-EPMC12717054 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature