Hyperglycemia-induced oxidative stress in the development of diabetic retinopathy

Authors

  • Ahmed Thabit Alnahdi Department of Ophthalmology, East Jeddah General Hospital, Jeddah, Saudi Arabia
  • Lama Abdulaziz Almujalli Riyadh First Health Cluster, Ministry of Health, Riyadh, Saudi Arabia
  • Sahar Yousef Alhawsawi Department of Ophthalmology, Hera General Hospital, Mecca, Saudi Arabia
  • Raneem Abdurabu Gomawi College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia
  • Abdullah Hazza Alhobera Hail Health Cluster, Ministry of Health, Hail, Saudi Arabia
  • Khawlah Fares Alshammari Department of Family Medicine, Hail Health Cluster, Hail, Saudi Arabia
  • Mazin Talal Alshammari Hail Health Cluster, Ministry of Health, Hail, Saudi Arabia
  • Hisham Muhammedeed Almuallim Department of Emergency Medicine, Ministry of Health, Jeddah, Saudi Arabia
  • Gehan Khalid Mubaraki College of Medicine, Alfaisal University, Riyadh, Saudi Arabia
  • Mansour Adel Shourbaji Department of Cardiology, Madinah General Hospital, Medina, Saudi Arabia

DOI:

https://doi.org/10.18203/2394-6040.ijcmph20250070

Keywords:

Diabetic retinopathy, Hyperglycemia, Oxidative stress, Inflammation, Mitochondrial dysfunction

Abstract

Diabetic retinopathy (DR), the leading cause of preventable blindness, is primarily caused by chronic hyperglycemia-induced oxidative stress. This review examines molecular mechanisms by which hyperglycemia-induced oxidative damage transmits into retinal tissue. We summarize the major pathways: polyol activation, advanced glycation end-products (AGEs), protein kinase C (PKC) dysregulation, and hexosamine pathway. Oxidative stress leads to mitochondrial dysfunction, apoptosis of retinal endothelium and pigment epithelium and activation of cytokines, as well as overexpression of vascular endothelial growth factor (VEGF). These processes together cause vascular leakage, macular edema and pathological angiogenesis. Trials of oxidative stress therapies (e.g. antioxidants, PKC inhibitors e.g., ruboxistaurin, and anti-VEGF agents e.g., ranibizumab, bevacizumab, aflibercept) as well as mitochondria targeted therapies are considered potential therapeutic approaches to improve DR prognosis. Further studies on DR pathophysiology and treatment are recommended to develop effective interventions for this vision threatening condition. Better prevention and management of DR requires early intervention and biomarker-based approaches.

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Published

2025-01-24

How to Cite

Thabit Alnahdi, A., Almujalli, L. A., Alhawsawi, S. Y., Gomawi, R. A., Alhobera, A. H., Alshammari, K. F., Alshammari, M. T., Almuallim, H. M., Mubaraki, G. K., & Shourbaji, M. A. (2025). Hyperglycemia-induced oxidative stress in the development of diabetic retinopathy. International Journal Of Community Medicine And Public Health, 12(2), 1066–1073. https://doi.org/10.18203/2394-6040.ijcmph20250070

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Review Articles