Role of Inflammation in Diabetic Retinopathy.

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Term Occurence Count Dictionary
Etanercept 1 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
diabetic retinopathy 13 endocrinologydiseases
hyperglycemia 6 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
Alexander disease 1 endocrinologydiseases

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Etanercept 55174 therapy has been studied in a few clinical cases. Patients with refractory DME treated with intravitreal Etanercept (TNFα inhibitor) showed no statistically significant improvement [[229]]. Infliximab, a TNFα neutralizing
Select Disease Character Offset Disease Term Instance
Alexander disease 48290 in glial cells, α-crystallins have been reported to be upregulated in astrocytes of patients with Alexander disease and microglial cells of patients with Alzheimer’s disease [[199],[200],[201]]. It has been hypothesized
diabetes mellitus 2097 the working-age population of the Western world [[1]]. Among microvascular complications related to diabetes mellitus such as nephropathy and neuropathy, DR is the most common. The prevalence rate for DR for all adults
diabetic retinopathy 614 diabetes and remains the leading cause of blindness among the working-age population. For decades, diabetic retinopathy was considered only a microvascular complication, but the retinal microvasculature is intimately associated
diabetic retinopathy 1002 vascular alterations, there is still no treatment to counteract the early neuro-glial perturbations in diabetic retinopathy . Diabetes is a complex metabolic disorder, characterized by chronic hyperglycemia along with dyslipidemia,
diabetic retinopathy 1697 response. In the current review, we focus on the involvement of inflammation in the pathophysiology of diabetic retinopathy with special emphasis on the functional relationships between glial cells and neurons. Finally, we summarize
diabetic retinopathy 1890 cells and neurons. Finally, we summarize recent advances using novel targets to inhibit inflammation in diabetic retinopathy .1. IntroductionDiabetic retinopathy (DR) is the primary cause of visual impairment in the working-age
diabetic retinopathy 6387 published in the last decade have summarized the evidence that neurons are vulnerable and die early in diabetic retinopathy , however, the pathophysiological mechanisms underlying this neurodegenerative process remain to be clearly
diabetic retinopathy 37138 restoring such function in DR could become a cornerstone for developing effective therapies to treat diabetic retinopathy .4.3. AstrocytesLike Müller cells, astrocytes are connected to retinal blood vessels and neurons and
diabetic retinopathy 44793 of pro-inflammatory factors [[185]]. Therefore, regulation of retinal function by AQP4 may attenuate diabetic retinopathy , offering a promising therapeutic strategy for diabetic retinopathy [[185]].Neurodegeneration leads
diabetic retinopathy 44861 function by AQP4 may attenuate diabetic retinopathy, offering a promising therapeutic strategy for diabetic retinopathy [[185]].Neurodegeneration leads to the alteration of expression of growth factors (e.g., VEGF) by glial
diabetic retinopathy 49026 development of specifically engineered crystallin proteins, which could be applied to the treatment of diabetic retinopathy and other neurodegenerative conditions.5.2. Matrix MetalloproteinasesMatrix metalloproteinases constitute
diabetic retinopathy 62009 molecular mechanisms underlying ocular inflammation in patients with DR.Figure 1Clinical features of diabetic retinopathy and causative pro-inflammatory chemokines. (A) A fundus photograph shows the right eye of a 57-year-old
diabetic retinopathy 62201 shows the right eye of a 57-year-old man with 20/80 visual acuity and signs of severe non-proliferative diabetic retinopathy with non-significant macular edema (the region of macular edema is indicated by the bracket). Vascular
diabetic retinopathy 62934 Protein.Figure 2Schematic representation of pathogenic mechanisms leading to sight-threatening endpoints of diabetic retinopathy (DR): proliferative DR (PDR) and diabetic macular edema (DME). Metabolic alterations are first sensed
diabetic retinopathy 64490 growth factors in the vitreous or aqueous humor of human diabetic patients with different stages of diabetic retinopathy (DR). If only information on serum levels were available, it is mentioned specifically. ↑ upregulation,
hyperglycemia 1091 perturbations in diabetic retinopathy. Diabetes is a complex metabolic disorder, characterized by chronic hyperglycemia along with dyslipidemia, hypoinsulinemia and hypertension. Increasing evidence points to inflammation
hyperglycemia 18463 primarily due to glucose-induced cytokine released by neighboring cells rather than a direct effect of hyperglycemia on endothelial cells themselves [[100]]. Upon cytokine stimulation they also secrete intracellular adhesion
hyperglycemia 25041 glucose treatment itself cannot be completely excluded, it has been demonstrated, that also in vivo hyperglycemia increased circulating cytokine concentrations by an oxidative mechanism in diabetic patients [[133]].
hyperglycemia 25189 concentrations by an oxidative mechanism in diabetic patients [[133]]. This suggests a causal role for hyperglycemia in the immune response associated with diabetes. In addition, immunohistochemical studies demonstrated
hyperglycemia 45776 exacerbating retinal neurodegeneration [[187]].Conversely a growing body of evidence indicates that hyperglycemia -induced downregulation of a number of important neurotrophic factors, such as NGF, Pigment epithelium-derived
hyperglycemia 46431 surface of RGCs [[189],[190]]. PEDF levels were found to be decreased in cultured MGCs subjected to hyperglycemia and mild hypoxia [[191],[192]]. However, under severe hypoxic conditions, PEDF was upregulated, potentially
hyperlipidemia 53084 development or progression of DR. Metabolic control (tight glycemic control, regulation of blood pressure and hyperlipidemia ) is associated with a lower risk of retinopathy [[218],[219]]. Specific therapeutic options for DR include

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