The Oxidative Stress and Mitochondrial Dysfunction during the Pathogenesis of Diabetic Retinopathy

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Term Occurence Count Dictionary
diabetic retinopathy 7 endocrinologydiseases
fenofibrate 1 endocrinologydiseasesdrugs
hyperglycemia 12 endocrinologydiseases
dexamethasone 2 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
dexamethasone 29689 [[106]].Ozurdex (Allergan, Irvine, California, USA) is a biodegradable implant that slowly releases 0.7 mg of dexamethasone over 6 months. The Macular Edema: Assessment of Implantable Dexamethasone in Diabetes (MEAD) study evaluated
dexamethasone 29833 Edema: Assessment of Implantable Dexamethasone in Diabetes (MEAD) study evaluated the effectiveness of dexamethasone implants in patients with DME. A higher percentage of patients was shown to achieve more than 15-letter
fenofibrate 34371 [[128]]. The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study reported the effects of fenofibrate on the cardiovascular system and the considerable decrease in the need for laser photocoagulation treatment
Select Disease Character Offset Disease Term Instance
diabetic retinopathy 1321 of ROS, local inflammation, and cell death are tightly linked and considerably affect all phases of diabetic retinopathy pathogenesis. Furthermore, microvascular dysfunction induces ischemia and local inflammation, leading
diabetic retinopathy 1654 Therefore, it is crucial to understand and elucidate the detailed mechanisms underlying the development of diabetic retinopathy . In this review, we summarized the existing knowledge about the pathogenesis and current strategies
diabetic retinopathy 1796 summarized the existing knowledge about the pathogenesis and current strategies for the treatment of diabetic retinopathy , and we believe this systematization will help and support further research in this area.1. IntroductionDiabetes
diabetic retinopathy 35573 DR development represents an important conceptual advance in this field.Figure 1Clinical feature of diabetic retinopathy , including microaneurysm, microhemorrhage, cotton wool spots, neovascularization, and hard exudates.Figure
diabetic retinopathy 35755 neovascularization, and hard exudates.Figure 2Illustration showing different mechanisms underlying diabetic retinopathy . During hyperglycemia, the excessive production of reactive oxygen species (ROS) via polyol pathway,
diabetic retinopathy 36273 vascular dysfunction operate in parallel and closely, which ultimately leads to the development of diabetic retinopathy .Figure 3Mechanisms underlying hyperglycemia-induced oxidative stress increase that is involved in diabetic
diabetic retinopathy 36392 retinopathy.Figure 3Mechanisms underlying hyperglycemia-induced oxidative stress increase that is involved in diabetic retinopathy pathogenesis
hyperglycemia 856 9/2018AbstractDiabetic retinopathy is one of the most serious microvascular complications induced by hyperglycemia via five major pathways, including polyol, hexosamine, protein kinase C, and angiotensin II pathways
hyperglycemia 1032 kinase C, and angiotensin II pathways and the accumulation of advanced glycation end products. The hyperglycemia -induced overproduction of reactive oxygen species (ROS) induces local inflammation, mitochondrial dysfunction,
hyperglycemia 1984 research in this area.1. IntroductionDiabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia , due to the defects in insulin secretion and impaired insulin resistance. Diabetes, the long-term high
hyperglycemia 6019 Mechanisms Underlying the Development and Progression of DRDR is a multifactorial disease, characterized by hyperglycemia , leukostasis, microvascular damage, microinflammation, increased vascular permeability, vascular occlusion,
hyperglycemia 6199 vascular permeability, vascular occlusion, local ischemia, and general neurodegeneration. Persistent hyperglycemia induces cellular metabolism imbalance, including excessive glucose oxidation, ROS production, local
hyperglycemia 6836 on the retinal capillaries, responsible for the balancing of vascular permeability, are damaged by hyperglycemia , which further leads to fluid leakage and accumulation in the retina due to the breakdown of tight junctions
hyperglycemia 8368 represent a key factor in this process [[16]]. Clinical and experimental studies demonstrated that hyperglycemia represents the primary factor leading to the pathogenesis of diabetic complications [[17]]. In the ischemic
hyperglycemia 9184 Polyol Pathway ActivationPolyol pathway activation represents one of the processes observed under the hyperglycemia -induced oxidative stress conditions during DR pathogenesis, and this pathway is known as the sorbitol-aldose
hyperglycemia 12312 intracellular factors [[30]]. The hexosamine pathway was reported to mediate the toxic effects of ROS in hyperglycemia [[28]–[31]]. In the presence of increased glucose levels, a large amount of ROS is generated, which
hyperglycemia 17492 which may lead to the retinal capillary cell apoptosis [[63]–[65]]. Oxidative stress increase during hyperglycemia damages the structure and function of mitochondria [[63]]. The main alterations in the expression levels
hyperglycemia 35784 exudates.Figure 2Illustration showing different mechanisms underlying diabetic retinopathy. During hyperglycemia , the excessive production of reactive oxygen species (ROS) via polyol pathway, advanced glycation end
hyperglycemia 36324 closely, which ultimately leads to the development of diabetic retinopathy.Figure 3Mechanisms underlying hyperglycemia -induced oxidative stress increase that is involved in diabetic retinopathy pathogenesis

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