Retinal ischemia: mechanisms of damage and potential therapeutic strategies

Osborne, Neville N.; Casson, Robert J.; Wood, J. K.; Chidlow, Glyn; Graham, Mark; Melena, José

doi:10.1016/j.preteyeres.2003.12.001

Cited by 901 publications

(888 citation statements)

References 485 publications

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“…Ischemia should be distinguished from simple anoxia (a complete lack of oxygen) or hypoxia (a reduction in oxygen) [9]. Hypoxia means a reduction of oxygen availability or utilization, and it may develop as a consequence of reduced oxygen supply, reduced ambient pO 2 , low hemoglobin or reduced tissue utilization caused by impairments in the mitochondrial cytochrome enzymes.…”

Section: Ischemic Retinamentioning

confidence: 99%

“…Retinal ischemia is a common clinical entity and, due to relatively ineffective treatment, remains a common cause of visual impairment and blindness [9-11]. Indeed, ischemia in the retina and optic nerve is assumed to be involved in the pathogenesis of major vision-threatening diseases, such as age-related macular degeneration, diabetic retinopathy and glaucoma.…”

Section: Ischemic Retinamentioning

confidence: 99%

See 1 more Smart Citation

The Neuropeptide Systems and their Potential Role in the Treatment of Mammalian Retinal Ischemia: A Developing Story

Cervia¹,

Casini²

2013

Current Neuropharmacology

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The multiplicity of peptidergic receptors and of the transduction pathways they activate offers the possibility of important advances in the development of specific drugs for clinical treatment of central nervous system disorders. Among them, retinal ischemia is a common clinical entity and, due to relatively ineffective treatment, remains a common cause of visual impairment and blindness. Ischemia is a primary cause of neuronal death, and it can be considered as a sort of final common pathway in retinal diseases leading to irreversible morphological damage and vision loss. Neuropeptides and their receptors are widely expressed in mammalian retinas, where they exert multifaceted functions both during development and in the mature animal. In particular, in recent years somatostatin and pituitary adenylate cyclase activating peptide have been reported to be highly protective against retinal cell death caused by ischemia, while data on opioid peptides, angiotensin II, and other peptides have also been published. This review provides a rationale for harnessing the peptidergic receptors as a potential target against retinal neuronal damages which occur during ischemic retinopathies.

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Section: Ischemic Retinamentioning

confidence: 99%

Section: Ischemic Retinamentioning

confidence: 99%

The Neuropeptide Systems and their Potential Role in the Treatment of Mammalian Retinal Ischemia: A Developing Story

Cervia¹,

Casini²

2013

Current Neuropharmacology

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“…Moreover, retinal I/R injury developed vision loss and even blindness, owing to eternal damage to the retina, particularly retinal neurons 3, 4, 5. Ischaemia blocked blood flow to retina, causing the transient deficiency of oxygen and other physiological nutrients, such as adenosine triphosphate 6.…”

Section: Introductionmentioning

confidence: 99%

Collagen peptide modified carboxymethyl cellulose as both antioxidant drug and carrier for drug delivery against retinal ischaemia/reperfusion injury

Mao

Wang

Wei

et al. 2018

J Cellular Molecular Medi

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Oxidative stress can cause injury in retinal endothelial cells. Carboxymethyl cellulose modified with collagen peptide (CMCC) is of a distinct antioxidant capacity and potentially a good drug carrier. In this study, the protective effects of CMCC against H2O2‐induced injury of primary retinal endothelial cells were investigated. In vitro, we demonstrated that CMCC significantly promoted viability of H2O2‐treated cells, efficiently restrained cellular reactive oxygen species (ROS) production and cell apoptosis. Then, the CMCC was employed as both drug and anti‐inflammatory drug carrier for treatment of retinal ischaemia/reperfusion (I/R) in rats. Animals were treated with CMCC or interleukin‐10‐loaded CMCC (IL‐10@CMCC), respectively. In comparisons, the IL‐10@CMCC treatment exhibited superior therapeutic effects, including better restoration of retinal structural thickness and less retinal apoptosis. Also, chemiluminescence demonstrated that transplantation of IL‐10@CMCC markedly reduced the retinal oxidative stress level compared with CMCC alone and potently recovered the activities of typical antioxidant enzymes, SOD and CAT. Therefore, it could be concluded that CMCC provides a promising platform to enhance the drug‐based therapy for I/R‐related retinal injury.

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“…Their role under pathologic conditions caused by mutations, ischemia or injuries is less well understood, they may exacerbate or mitigate neuronal damage. Extracellular accumulation of glutamate, the major neurotransmitter in the CNS, damages neurons in different pathologies including ischemia (Brassai, Suvanjeiev, Bán, & Lakatos, 2015; Osborne et al, 2004), but the contribution of glial cells remains unclear (Rossi & Volterra, 2009). Under normal conditions, glial cells control the extracellular glutamate concentration by electrogenic glutamate transporters (Bringmann et al, 2013; Grewer & Rauen, 2005; Rauen, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…Here, we studied the contribution of glial SNARE‐dependent exocytosis to neurodegeneration in the retina. To this end, we used an established model of transient ischemia that triggers robust neuronal dysfunction and degeneration (Osborne et al, 2004; Pannicke et al, 2014). To interfere with glial exocytosis, we used a mouse line enabling inducible expression of a dominant‐negative domain of synaptobrevin (dnSNARE mice; Pascual et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Suppression of SNARE‐dependent exocytosis in retinal glial cells and its effect on ischemia‐induced neurodegeneration

Wagner

Pannicke

Rupprecht

et al. 2017

Glia

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Nervous tissue is characterized by a tight structural association between glial cells and neurons. It is well known that glial cells support neuronal functions, but their role under pathologic conditions is less well understood. Here, we addressed this question in vivo using an experimental model of retinal ischemia and transgenic mice for glia‐specific inhibition of soluble N‐ethylmaleimide‐sensitive factor attachment protein receptor (SNARE)‐dependent exocytosis. Transgene expression reduced glutamate, but not ATP release from single Müller cells, impaired glial volume regulation under normal conditions and reduced neuronal dysfunction and death in the inner retina during the early stages of ischemia. Our study reveals that the SNARE‐dependent exocytosis in glial cells contributes to neurotoxicity during ischemia in vivo and suggests glial exocytosis as a target for therapeutic approaches.

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Retinal ischemia: mechanisms of damage and potential therapeutic strategies

Cited by 901 publications

References 485 publications

The Neuropeptide Systems and their Potential Role in the Treatment of Mammalian Retinal Ischemia: A Developing Story

The Neuropeptide Systems and their Potential Role in the Treatment of Mammalian Retinal Ischemia: A Developing Story

Collagen peptide modified carboxymethyl cellulose as both antioxidant drug and carrier for drug delivery against retinal ischaemia/reperfusion injury

Suppression of SNARE‐dependent exocytosis in retinal glial cells and its effect on ischemia‐induced neurodegeneration

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