Key points are not available for this paper at this time.
Retinal ganglion cells (RGCs) are the visual gateway of the brain, with their axons converging to form the optic nerve, making them the most vulnerable target in diseases such as glaucoma and traumatic optic neuropathy (TON). In both diseases, the disruption of the blood-retinal barrier(BRB) is considered an important mechanism that accelerates RGC degeneration and hinders axon regeneration. The BRB consists of the inner blood-retinal barrier (iBRB) and the outer blood-retinal barrier (oBRB), which are maintained by endothelial cells(ECs), pericytes(PCs), and retinal pigment epithelial (RPE), respectively. Their functions include regulating nutrient exchange, oxidative stress, and the immune microenvironment. However, in glaucoma and TON, the structural and functional integrity of the BRB is severely damaged due to mechanical stress, inflammatory reactions, and metabolic disorders. Emerging evidence highlights that BRB disruption leads to heightened vascular permeability, immune cell infiltration, and sustained chronic inflammation, creating a hostile microenvironment for RGC survival. Furthermore, the dynamic interplay and imbalance among ECs, PCs, and glial cells within the neurovascular unit (NVU) are pivotal drivers of BRB destruction, exacerbating RGC apoptosis and limiting optic nerve regeneration. The intricate molecular and cellular mechanisms underlying these processes underscore the BRB's critical role in glaucoma and TON pathophysiology while offering a compelling foundation for therapeutic strategies targeting BRB repair and stabilization. This review provides crucial insights and lays a robust groundwork for advancing research on neural regeneration and innovative optic nerve protective strategies.
Zhou et al. (Wed,) studied this question.