A phenome-wide Mendelian randomisation analysis revealed a causal link between age-related macular degeneration and a number of lipid, complement, immune cell, and serum protein traits, highlighting potential treatment targets.

The IL-4/IL-4Rα axis directory promotes pathological angiogenesis through communications with bone marrow cells leading to neovascular age-related macular degeneration.

The eye produces a protein that inhibits the growth of blood vessels in the deep retina, which includes the photoreceptor layer, and disruption of this process can lead to blindness.

TGFβ signaling to retinal microglia is central to the regulation of neuroinflammatory responses relevant to age-related macular degeneration (AMD), a leading cause of blindness in the developed world.

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.

lncEGFL7OS is a lncRNA located at the EGFL7/miR-126 locus that is critical for angiogenesis in humans.

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.

Pathological vessel leakage in mouse retinopathy models depends on VE-cadherin Y685 phosphorylation status, which in turn is regulated by a signaling cascade originating with VEGFR2 Y949 phosphorylation.

IL-1β release from macrophages might be responsible for the unexplained cone segment loss in retinal degenerative diseases that are associated with subretinal inflammation, such as retinitis pigmentosa or geographic atrophy.