ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Dual-Target ROS-Driven Spatiotemporal Senolysis for Vascular Repair and Immune Microenvironment Reprogramming in the Treatment of Ocular Fundus Neovascularization.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
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Authors and funding
11 authors.
Funding
Abstract
Ocular fundus neovascularization (OFN) is a leading cause of irreversible vision loss. Conventional antivascular endothelial growth factor (anti-VEGF) therapies indiscriminately suppress pathological and reparative angiogenesis and fail to correct the senescence- and inflammation-driven microenvironment that sustains disease progression. Senescent endothelial cells (ECs) form the structural scaffold of pathological vessels, while neighboring senescent microglia exacerbate inflammatory signaling, together deteriorating the reactive oxygen species (ROS)-rich vascular-immune microenvironment. Here, we develop an injectable ROS-responsive senolytic hydrogel (PCC1/PHCF-Gel) that enables lesion-activated, sustained intraocular release of procyanidin C1 (PCC1), overcoming rapid clearance, oxidative degradation, and poor lesion retention associated with free PCC1. In oxygen-induced retinopathy and choroidal neovascularization models, PCC1/PHCF-Gel markedly reduces retinal senescence, suppresses pathological neovascularization, and restores neuroretinal function, outperforming symptom-directed therapies anti-VEGF therapy. Single-cell RNA sequencing reveals selective elimination of two pathogenic senescent cell subpopulations-CXCR4
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