SynthesisInternational ophthalmology2025
Exploring the role of oxidative stress in retinal vein occlusion: an updated and comprehensive review on the pathophysiology and treatment perspectives.
Synthesis in International ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Early Real-World Experience of Switching to Faricimab for Macular Oedema Secondary to Vein Occlusion.Life (Basel, Switzerland) · 2026Article
- Involvement of Oxidative Stress-Related Inflammatory Mediators in the Pathogenesis and Treatment Response of Macular Edema Secondary to Branch Retinal Vein Occlusion.Antioxidants (Basel, Switzerland) · 2026Article
- Pathophysiological Roles of Oxidative Stress and the Translational Potential of Antioxidant Therapy in Retinal Vein Occlusion.Antioxidants (Basel, Switzerland) · 2026Review
- Intravitreal Dexamethasone Implant in Retinal Vein Occlusion: A Pilot Study Exploring Baseline Ocular and Circulating Biomarkers.International journal of molecular sciences · 2026Article
- Impact of Comorbid Hypertension and Diabetes on Anti-VEGF Treatment Outcomes in Macular Edema.Journal of ophthalmology · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
introductionRetinal vein occlusion (RVO) represents a prevalent cause of vision impairment within retinal vascular diseases. Although hypoperfusion and inflammation are recognized pathogenic contributors, emerging evidence highlights oxidative stress as a pivotal mediator operating through ischemia-hypoxia-inflammation cascades.
methodsWe conducted a systematic review of preclinical models and clinical studies examining reactive oxygen species (ROS) mechanisms in RVO pathogenesis. We searched PubMed/MEDLINE
resultsIn ischemic retina, ROS accumulation stabilizes hypoxia-inducible factor-1α (HIF-1α) and induces vascular endothelial growth factor (VEGF) expression, promoting vascular hyperpermeability and proinflammatory cytokine release. Bidirectional interactions between ROS signaling and systemic vascular mediators, including hypertension and the renin-angiotensin-aldosterone system (RAAS), disrupt redox homeostasis, increase retinal venous pressure, and impair microvascular perfusion. Oxidative stress-mediated activation of resident microglia and infiltrating macrophages promotes tight-junction protein degradation, resulting in blood-retinal barrier (BRB) breakdown and subsequent neurovascular injury. Patients with elevated systemic oxidative burden frequently present with bilateral, subclinical retinal microvascular impairment. Targeted antioxidant interventions, including nanoparticle-based delivery systems and bioactive phytochemicals, demonstrated efficacy in preclinical models by restoring redox balance, preserving BRB integrity, and reducing neurovascular damage.
conclusionOxidative stress represents a critical factor in RVO progression through interconnected vascular, inflammatory, and immune pathways. We propose a comprehensive management framework incorporating multimodal imaging for oxidative biomarker detection, artificial intelligence implementation for risk stratification, and personalized antioxidant therapy guided by validated biomarkers. Future investigations must establish causal relationships and identify specific, noninvasive biomarkers to advance precision prevention and treatment strategies for RVO.
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Identifiers
40875080What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.