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Oxidative Stress and Diabetic Retinopathy

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Oxidative Stress and Diabetic Retinopathy Eye (2017) 31, 1122–1130 © 2017 Macmillan Publishers Limited, part of Springer Nature. All rights reserved 0950-222X/17 www.nature.com/eye 1 2,3,4 2,4 REVIEW Oxidative stress and GD Calderon , OH Juarez , GE Hernandez , 2,4 3,4 diabetic retinopathy: SM Punzo and ZD De la Cruz development and treatment Abstract Diabetic retinopathy (DR) is the most common time thus, DR is a time-dependent disease that microvascular complication in diabetic patients develops in stages. The incidence increases to and one of the main causes of acquired 50% at 10 years after the diagnosis of diabetes, blindness in the world. From the 90s until date, and goes up to 90% at 25 years. These figures put the incidence of this complication has this complication as the most common increased. Reactive oxygen species (ROS) is a microvascular complication in diabetic patients free radical with impaired electron that usually and one of the major causes of acquired participates in the redox mechanisms of some blindness in the world. This increase in body molecules such as enzymes, proteins, and prevalence may be attributed to prolonged so on. In normal biological conditions, ROS is survival of diabetic patients. In the United maintained in equilibrium, however its over- States, it is the leading cause of blindness among 1 Laboratory of production can lead to biological process called adults aged 20–74 years.1 The more advanced Neurochemistry, National oxidative stress and this is considered the main form of DR is diabetic macular edema (DME), Institute of Pediatrics, pathogenesis of DR. The retina is susceptible fi Mexico City, Mexico which signi cantly increases the risk of to ROS because of high-energy demands and blindness. Diabetic maculopathy is the result of 2Laboratory of exposure to light. When the balance is broken, multifactorial and complex alterations of the Pharmacology, National ROS produces retinal cell injury by interacting retinal capillaries in association with diabetes Institute of Pediatrics, with the cellular components. This article mellitus and it is divided into two forms, Mexico City, Mexico describes the possible role of oxidative stress ischemic maculopathy and DME.2 The high in the development of DR and proposes some 3 mortality and morbidity caused by diabetes is as Faculty of Medicine, treatment options based on its stages. The Department of a result of its vascular complications. Pharmacology, National review of the topic shows that blindness Two of the complications of DR that threaten Autonomous University of caused by DR can be avoided by early the vision of the patients are DME and Mexico, Mexico City, detection and timely treatment. proliferative DR.3 Patients with DM2 usually Mexico Eye (2017) 31, 1122–1130; doi:10.1038/eye.2017.64; begin to develop retinopathy 7 years after published online 28 April 2017 4 Correspondence: diagnosis of the disease. OH Juarez, Laboratory of Naruse et al5 suggests that DR cause reactive Pharmacology, National oxygen species (ROS) to increase the level of Institute of Pediatrics, Av reactive oxygen metabolites. Catabolites of Imán #1, 3er piso, Col Cuicuilco, Mexico City CP biomolecules such as nitric oxide (NO), catalase, 04530, Mexico Diabetic retinopathy glutathione peroxide, and lipoperoxide increase Tel: +52 55 10843883; with the progression of DR in DM2 patients.6 Fax: +52 55 10843883. According to WHO, diabetes mellitus is a High glucose level and diabetically induced E-mail: [email protected] chronic degenerative disease that occurs when activation of retinal vascularization is linked or [email protected] the pancreas does not produce enough insulin or with elevation in the enzymatic activity of when the body does not effectively use the 4These authors contributed arginase as well as in the reduction of equally to this work. insulin produced by the pancreas. The high bioavailability of NO.7 The over activity of mortality and morbidity caused by diabetes is as arginase plays an important role in the Received: 27 November a result of its vascular complications. development of DR through its reducing effect 2015 Approximately 400 million people worldwide on NO and increase of oxidative stress. One of Accepted in revised form: have type 2 diabetes, and more than 45% of 14 March 2017 the pathways for the generation of NO is Published online: 28 April them have diabetic retinopathy (DR). The through the activity of inducible nitric oxide 2017 progress of diabetes to retinopathy happens over synthase, an isoform of NOS. This enzyme acts Oxidative stress and retinopathy GD Calderon et al 1123 on 1-arginine and converts it to 1-citrulline.8 development of the disorder.16 In vascular inflammation, NO produced from S-nitrosoglutathione (GSNO) plays a the involvement of biomolecules as lipoprotein-PLA2, second messenger role and regulates the activity and pro-inflammatory cytokines (TNF-alpha and IL-1), and expression of some proteins by A-nitrosylation and hence secretory phospholipase A2 IIA has been pinpointed.17 plays vital role in many cellular processes. It is involved Since the underlying problem in this pathology is the in physiological functions such as vasodilation, high levels of blood glucose, the progressive damage can neurotransmission, and host defense. be retarded or completely abated by intensive insulin therapy. In addition, to reduce pericytic cell death, it has been found that thioredoxin, a novel gene and drug, is a Diabetic retinopathy mechanism potent therapeutic agent to prevent pericytic cell death In the biosynthetic pathway of hexosamine, there is an and DR progression.18 Moreover, a comprehensive increase in the activity of dumping of post-translational knowledge of cytokine-induced changes in lipid modifications of Ser/Thr residues through O-linked metabolism will promote the development of novel β-N-acetylglucosamine (O-GlcNAc). This increased influx concepts and steer bench-to-bedside therapeutic of residues is dumped on the proteins and thus, reduce developments.18 their capacity to capture the blood glucose and in this way leads to diabetes. It is known that as in protein Screening and gene expression phosphorylation, O-GlcN acylation plays a regulatory role in many nuclear and cytoplasmic proteins.9 The DR prevention lies on its timely diagnosis achieved by a development of different vascular complications (macro well-established medical care delivery plan based on a and micro) is one of the key risks of suffering from well-implemented screening program for the detection of diabetes and in the ocular regions, and these its onset and its prompt medical treatment to reduce the complications usually culminate in DR.10 incidence of radical management (vitrectomy) and DR is the principal cause of blindness in working blindness.19 British Diabetic Association established a adults. The mechanism underlying this is the standard value for DR screening program with a inflammation of the retinal blood vessel caused by deposit sensitivity of 80 and specificity of 95%, and has created a of arteriosclerotic plates produced by excess blood world record in DR screening with a coverage of 85.7%. glucose and thus making them susceptible to Chromosome 21 has a protective effect against DR as microrupture leading to the leakage of fluids into the seen in Down’s syndrome patients with three copies of retina. If unchecked, there is a growth of new vessels that the chromosome and high level of endostatin, an anti- distorts the microvasculature of the retina and this angiogenic protein from collagen XVIII whose gene is eventually provokes retinal detachment.11,12 located in the chromosome 21.20 Patients with deleterious The crucial point in the pathogenesis of the disease is polymorphisms in the uncoupling protein 1 (UCP1) have inflammation in addition with oxidative stress.13 Its a high risk of developing DR. In type I diabetic patients, progress is characterized by loss of neuronal and pericytic the expression of this protein occurs in the retina and cells that gives rise to growth of acellular-occluded impacts downwardly in the production of ROS by the capillaries. Such occlusion leads to the formation of mitochondria. This was confirmed in a study carried out microaneurysms and hence increased leucostasis by Brondani et al,21 where it was reported that 3826A/G resulting to the thickening of basal vascular membrane. polymorphism affects UCP1 expression and decreases The loss of pericyte cells begins with the stimulation of mitochondrial production of ROS. There is high energy PKC-δ signaling by high level of blood glucose. This consumption in the molecular pathways that contribute to signaling cascade enhances the expression of protein retinal signal transduction with its consequences on the kinase C-δ (PKC-δ, encoded by Prkcd) and p38 mitogen- structure and function of this organ.22 Such elevated activated protein kinase, and dephosphorylates PDGF metabolic rates in the retina together with the receptors and diminishes its downstream signaling and vascularization play a part in the oxidative stress and thus brings about apoptotic death of the pericytic cells.14 influence age-related processes. In this way, high-energy The pericytic cell death gradually changes the architecture demand increases the oxidative load and enhances, in of the microvessels of the retina, a situation that provokes chronic manner, the increase of oxidative stress and ROS the collapse of blood–retinal barrier and hence extensive to impressive levels. The frequent exposure of the eye to bleeding, microaneurysms
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