Notch signaling in anti-VEGF resistant arteriolar choroidal neovascularization.

Authors

Jingwei Ding, Liwen Su, Wenjing Chen, Ronghan Wu, Ling Gao

Published in

Biochemical pharmacology. Pages 118214. Jul 04, 2026. Epub Jul 04, 2026.

Abstract

Choroidal neovascularization (CNV) is a major pathological hallmark of fundus diseases, such as age-related macular degeneration, and is commonly treated with anti-vascular endothelial growth factor (VEGF) agents. However, resistance to or a suboptimal response to anti-VEGF therapy, particularly in arteriolar CNV, remains a significant clinical challenge. Arteriolar CNV, characterized by arterialized vessels, feeding arterioles with high blood flow, and prominent fibrosis, remains persistently active and responds poorly to standard anti-VEGF therapy. Notch signaling confers anti VEGF resistance in various diseases including cancer and corneal neovascularization. However, its role in anti-VEGF resistant arteriolar CNV has not been systematically summarized. This review highlights Notch signaling as a key regulator of both physiological and pathological arterial remodeling, driving arteriolar differentiation and contributing to resistance to VEGF inhibitors. In tumors, Notch signaling plays a crucial role in driving arteriolar neovessel formation, promoting macrophage-mediated vascular remodeling, and enhancing fibrosis, all of which contribute to anti-VEGF resistance. We also discuss whether and how similar mechanisms may operate in arteriolar CNV and proposes that Notch signaling represents a potential therapeutic target. Furthermore,combining Notch inhibitors with anti-VEGF therapy may improve outcomes in patients with arteriolar CNV resistant to anti-VEGF therapy, thereby providing a potential therapeutic strategies. Future studies are warranted to elucidate the specific roles of Notch signaling in CNV and optimize therapeutic strategies for improved safety and efficacy.

PMID:
42401373
Bibliographic data and abstract were imported from PubMed on 05 Jul 2026.

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