Erythropoietin: when liability becomes asset in neurovascular repair

Grant, Maria B.; Boulton, Michael E.; Ljubimov, Alexander V.

doi:10.1172/jci34643

Cited by 12 publications

(10 citation statements)

References 38 publications

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“…Furthermore, EPO prevents glucose- and free radical-induced apoptosis of retinal cells [ 112 – 114 ]. However, EPO also has the undesirable property of potently stimulating neovascularization [ 101 , 115 ]. The interactions between VEGF and EPO in the eyes of patients with PDR have not been fully elucidated.…”

Section: Growth Factorsmentioning

confidence: 99%

Diabetic Retinopathy: Vascular and Inflammatory Disease

Semeraro

Cancarini

dell’Omo

et al. 2015

Journal of Diabetes Research

333

268

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Diabetic retinopathy (DR) is the leading cause of visual impairment in the working-age population of the Western world. The pathogenesis of DR is complex and several vascular, inflammatory, and neuronal mechanisms are involved. Inflammation mediates structural and molecular alterations associated with DR. However, the molecular mechanisms underlying the inflammatory pathways associated with DR are not completely characterized. Previous studies indicate that tissue hypoxia and dysregulation of immune responses associated with diabetes mellitus can induce increased expression of numerous vitreous mediators responsible for DR development. Thus, analysis of vitreous humor obtained from diabetic patients has made it possible to identify some of the mediators (cytokines, chemokines, and other factors) responsible for DR pathogenesis. Further studies are needed to better understand the relationship between inflammation and DR. Herein the main vitreous-related factors triggering the occurrence of retinal complication in diabetes are highlighted.

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Section: Growth Factorsmentioning

confidence: 99%

Diabetic Retinopathy: Vascular and Inflammatory Disease

Semeraro

Cancarini

dell’Omo

et al. 2015

Journal of Diabetes Research

333

268

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show abstract

“…In contrast, if EPO is administered in the normoxic period when endogenous EPO is elevated, neoangiogenesis is amplified. Thus, timing of administration with respect to the pathophysiology is of the utmost importance in some disease states [92].…”

Section: Efficacy Of Peripherally Administered Epo In Neurological DImentioning

confidence: 99%

Erythropoietin‐mediated tissue protection: reducing collateral damage from the primary injury response

Brines¹,

Cerami²

2008

Journal of Internal Medicine

302

378

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“…Erythropoietin (Epo) is another potent neuroprotective factor synthesized in the retina [ 57 , 58 ]. In addition to neuroprotection, Epo helps in the mobilization of endothelial progenitor cells (EPCs) toward injured retinal sites, thus involves in the neurovascular repair [ 59 , 60 ]. Therefore, a better understanding of the molecular mechanism and function of neurotrophins in the retina is necessary which may contribute as therapeutic agents in neuroprotection.…”

Section: Dysregulation Of Neurotrophins In Diabetic Retinamentioning

confidence: 99%

Neurodegeneration in Diabetic Retina and Its Potential Drug Targets

Ola¹,

Alhomida

2014

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Diabetic retinopathy (DR) is one of the major complications of diabetes causing vision loss and blindness worldwide. DR is widely recognized as a neurodegenerative disease as evidenced from early changes at cellular and molecular levels in the neuronal component of the diabetic retina, which is further supported by various retinal functional tests indicating functional deficits in the retina soon after diabetes progression. Diabetes alters the level of a number of neurodegenerative metabolites, which increases influx through several metabolic pathways which in turn induce an increase in oxidative stress and a decrease in neurotrophic factors, thereby damage retinal neurons. Loss of neurons may implicate in vascular pathology, a clinical signs of DR observed at later stages of the disease. Here, we discuss diabetes-induced potential metabolites known to be detrimental to neuronal damage and their mechanism of action. In addition, we highlight important neurotrophic factors, whose level have been found to be dysregulated in diabetic retina and may damage neurons. Furthermore, we discuss potential drugs and strategies based on targeting diabetes-induced metabolites, metabolic pathways, oxidative stress, and neurotrophins to protect retinal neurons, which may ameliorate vision loss and vascular damage in DR.

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Erythropoietin: when liability becomes asset in neurovascular repair

Cited by 12 publications

References 38 publications

Diabetic Retinopathy: Vascular and Inflammatory Disease

Diabetic Retinopathy: Vascular and Inflammatory Disease

Erythropoietin‐mediated tissue protection: reducing collateral damage from the primary injury response

Neurodegeneration in Diabetic Retina and Its Potential Drug Targets

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