{"title":"Diabetic retinopathy as a sentinel of systemic vascular dysfunction: Shared molecular mechanisms with cardiovascular disease","authors":"Ting Wang, Hongyu Li, Chuyao Wang, Xiuyun Li, Aijun Deng, Xinwei Jiao","doi":"10.1016/j.exer.2025.110644","DOIUrl":null,"url":null,"abstract":"<div><div>Diabetic retinopathy (DR) and cardiovascular disease (CVD) represent interconnected complications of diabetes, bound by overlapping pathophysiological processes and epidemiological correlations. This review explores their interplay, highlighting hyperglycemia-driven oxidative stress, chronic inflammation, endothelial dysfunction, and advanced glycation end-products (AGEs)-receptor for AGEs (RAGE) axis activation, which contribute to retinal microvascular damage and systemic atherosclerosis. Severe DR markedly increases CVD risk, positioning it as a marker of vascular pathology. Therapies targeting these pathways, including intensive glycemic control, glucagon-like peptide-1 receptor agonists (GLP-1RAs), sodium-glucose cotransporter-2 inhibitors (SGLT2is), fenofibrate, and renin-angiotensin-aldosterone system (RAAS) inhibitors, offer dual benefits, slowing DR progression and reducing CVD events. Multidisciplinary strategies integrating retinal screening with CVD risk management enhance patient care. Challenges include clarifying causality and improving risk tools. Future research should prioritize causal mechanisms, biomarkers, and personalized treatments to prevent vision loss and cardiovascular morbidity in diabetes.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"261 ","pages":"Article 110644"},"PeriodicalIF":2.7000,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental eye research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0014483525004166","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"OPHTHALMOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Diabetic retinopathy (DR) and cardiovascular disease (CVD) represent interconnected complications of diabetes, bound by overlapping pathophysiological processes and epidemiological correlations. This review explores their interplay, highlighting hyperglycemia-driven oxidative stress, chronic inflammation, endothelial dysfunction, and advanced glycation end-products (AGEs)-receptor for AGEs (RAGE) axis activation, which contribute to retinal microvascular damage and systemic atherosclerosis. Severe DR markedly increases CVD risk, positioning it as a marker of vascular pathology. Therapies targeting these pathways, including intensive glycemic control, glucagon-like peptide-1 receptor agonists (GLP-1RAs), sodium-glucose cotransporter-2 inhibitors (SGLT2is), fenofibrate, and renin-angiotensin-aldosterone system (RAAS) inhibitors, offer dual benefits, slowing DR progression and reducing CVD events. Multidisciplinary strategies integrating retinal screening with CVD risk management enhance patient care. Challenges include clarifying causality and improving risk tools. Future research should prioritize causal mechanisms, biomarkers, and personalized treatments to prevent vision loss and cardiovascular morbidity in diabetes.
期刊介绍:
The primary goal of Experimental Eye Research is to publish original research papers on all aspects of experimental biology of the eye and ocular tissues that seek to define the mechanisms of normal function and/or disease. Studies of ocular tissues that encompass the disciplines of cell biology, developmental biology, genetics, molecular biology, physiology, biochemistry, biophysics, immunology or microbiology are most welcomed. Manuscripts that are purely clinical or in a surgical area of ophthalmology are not appropriate for submission to Experimental Eye Research and if received will be returned without review.