C1q limits cystoid edema by maintaining basal beta-catenin-dependent signaling and blood-retina barrier function.

ABSTRACT: Macular edema (ME) causes significant vision impairment and occurs in several prevalent retinal diseases including diabetic retinopathy (DR), choroidal neovascularization (CNV), retinal vein occlusion, and uveitis. Retinal edema typically results from dysfunction of the blood-retina barrier (BRB), which is associated with increased retinal expression of complement components. It is unclear whether the classical complement pathway has detrimental or protective roles in the context of BRB dysfunction. Here, we characterize Tspan12 KO^DBM (Disrupted Barrier Maintenance) mice, a new mouse model of cystoid edema based on genetically and pharmacologically manipulating beta-catenin-dependent norrin/frizzled4 (FZD4) signaling. We assess BRB function, cystoid edema, ERG, and microg

SUBMITTER: Zhang L 

PROVIDER: S-EPMC12330627 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature