Inflammation, Fibrosis and Neovascularisation: New Perspectives for Old Foes in the Pathogenesis of Neovascular AMD

Dear Colleagues,

Choroidal neovascularisation manifests in advanced macular degeneration as a pathological growth of blood vessels in the choroid. The new blood vessel growth resulting from the choroid is leaky and, if untreated, leads to severe vision loss. Choroidal neovascularisation is akin to a maladaptive wound-healing response. The remodeled choroidal tissue environment is fibrotic and pro-inflammatory. Treatments that target neovascular-promoting factors (e.g., vascular endothelial growth factor and angiopoietin) have revolutionised our ability to prevent vision loss in neovascular macular degeneration. However, vision loss can continue to occur as treatments are unable to treat the subretinal fibrosis and inflammation that accompanies choroidal neovascularisation. Improving our understanding of the molecular processes that underpin these responses is, therefore, crucial to help ameliorate vision loss in neovascular macular degeneration.

For this Special Issue, we would like to invite papers that investigate and discuss the molecular signaling that drives choroidal neovascularisation pathogenesis and/or diagnosis or treatments. Suggested areas are molecular mechanisms of neovascularisation, fibrosis, and inflammation that regulate choroidal neovascularisation in preclinical or clinical settings. This includes novel treatment approaches that target or incorporate gene and cell therapies for choroidal neovascularization and identification or proposal of potential biomarkers (e.g., imaging, blood, or eye fluid) that are either implicated or associated with choroidal neovascularisation. Clinical research that includes molecular mechanism studies will also be welcomed.

Dr. Alice Brandli
Dr. Matt Rutar
Dr. Helder Andre
Guest Editors

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