Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications
By Qingzheng Kang, Chunxue Yang. Redox Biology, 2020
903 citations recorded by the source corpus.
Oxidative stress, a cytopathic outcome of excessive generation of ROS and the repression of antioxidant defense system for ROS elimination, is involved in the pathogenesis of multiple diseases, including diabetes and its complications. Retinopathy, a microvascular complication of diabetes, is the primary cause of acquired blindness in diabetic patients. Oxidative stress has been verified as one critical contributor to the pathogenesis of diabetic retinopathy. Oxidative stress can both contribute to and result from the metabolic abnormalities induced by hyperglycemia, mainly including the increased flux of the polyol pathway and hexosamine pathway, the hyper-activation of protein kinase C (PKC) isoforms, and the accumulation of advanced glycation end products (AGEs). Moreover, the repression of the antioxidant defense system by hyperglycemia-mediated epigenetic modification also leads to the imbalance between the scavenging and production of ROS. Excessive accumulation of ROS induces mitochondrial damage, cellular apoptosis, inflammation, lipid peroxidation, and structural and functional alterations in retina. Therefore, it is important to understand and elucidate the oxidative stress-related mechanisms underlying the progress of diabetic retinopathy. In addition, the abnormalities correlated with oxidative stress provide multiple potential therapeutic targets to develop safe and effective treatments for diabetic retinopathy. Here, we also summarized the main antioxidant therapeutic strategies to control this disease.
Subfields: Clinical Biochemistry, Neurology, Ophthalmology
View Paper: https://www.semanticscholar.org/paper/c7264d16e70cb43093593368ab1baefce2b1afc8
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In Clinical Biochemistry
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In Ophthalmology
Citations in the corpus
- Diabetic vascular diseases: molecular mechanisms and therapeutic strategies (2023, background): “Chronic hyperglycemia causes oxidative stress mainly through PKC, polyol, hexosamine, and AGEs formation pathways.(225) Hyperglycemia can regulate vascular cell permeability, the extracellular matrix, cell growth, neovascularization, cytokine response, and leukocyte adhesion through the diacylglycer”
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances (2025, positive): “Diabetes promotes raised mitochondrial damage and ROS production to retinal microvessels, leading to corresponding in fl ammation and oxidative stress which induces DR. 434 – 436 During hyperglycemia, retinal mitochondria experience alterations in mitochondrial membrane potential and an increase of m”
- Hyperglycemia and Oxidative Stress: An Integral, Updated and Critical Overview of Their Metabolic Interconnections (2023, background): “Recent reviews emphasizing the close association between hyperglycemia, oxidative stress and inflammation have been published in a number of human metabolic dysfunctions and pathologies related to the liver [15,16], adipose tissue [17], skeletal muscle [18,19], kidney [20,21], cardiovascular system ”