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A correlation between oxidative stress and diabetic retinopathy: An updated review
Afzal Hussain1, Sumel Ashique2, Obaid Afzal3
1Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh, 11451, Saudi Arabia.
Abstract:
Oxidative stress (OS) is a cytopathic outcome of excessively generated reactive oxygen species (ROS), down regulated antioxidant defense signaling pathways, and the imbalance between the produced radicals and their clearance. It plays a role in the genesis of several illnesses, especially hyperglycemia and its effects. Diabetic retinal illness, a micro vascular side effect of the condition, is the prime reason of diabetic related blindness. The OS (directly or indirectly) is associated with diabetic retinopathy (DR) and related consequences. The OS is responsible to induce and interfere the metabolic signaling pathways to enhance influx of the polyol cascades and hexosamine pathways, stimulate Protein Kinase-C (PKC) variants, and accumulate advanced glycation end products (AGEs). Additionally, the inequity between the scavenging and generation of ROS is caused by the epigenetic alteration caused by hyperglycemia that suppresses the antioxidant defense system. Induced by an excessive buildup of ROS, retinal changes in structure and function include mitochondrial damage, cellular death, inflammation, and lipid peroxidation. Therefore, it is crucial to comprehend and clarify the mechanisms connected to oxidative stress that underlie the development of DR.
Insights
Oxidative stress (OS) contributes to diabetic retinopathy (DR) by generating excess reactive oxygen species (ROS) and impairing antioxidant defenses. Understanding these mechanisms is key to preventing diabetic blindness.
Area of Science:
- Biochemistry
- Ophthalmology
- Pathophysiology
Background:
- Oxidative stress (OS) results from an imbalance between reactive oxygen species (ROS) generation and antioxidant defenses.
- OS is implicated in hyperglycemia and its complications, notably diabetic retinopathy (DR), a leading cause of blindness.
Purpose of the Study:
- To elucidate the mechanisms by which oxidative stress contributes to the development of diabetic retinopathy.
- To clarify the role of ROS, antioxidant system dysfunction, and metabolic pathway alterations in DR pathogenesis.
Main Methods:
- Review and synthesis of existing literature on oxidative stress and diabetic retinopathy.
- Analysis of molecular pathways affected by hyperglycemia and ROS, including polyol and hexosamine pathways, Protein Kinase-C (PKC), and advanced glycation end products (AGEs).
Main Results:
- Hyperglycemia-induced epigenetic alterations suppress the antioxidant defense system, exacerbating ROS accumulation.
- Oxidative stress promotes retinal structural and functional changes, including mitochondrial damage, apoptosis, inflammation, and lipid peroxidation.
- OS interferes with metabolic signaling, leading to increased polyol and hexosamine flux and PKC activation.
Conclusions:
- Oxidative stress is a critical factor in the pathogenesis of diabetic retinopathy.
- Targeting oxidative stress and restoring antioxidant balance may offer therapeutic strategies for preventing or treating DR and preserving vision.
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