Erythropoietin alleviates post-ischemic injury of rat hearts by attenuating nitrosative stress

Lu, Ming Jen; Chen, Yih‐Sharng; Huang, Huey W.; Chieh, Ming

doi:10.1016/j.lfs.2012.04.012

Cited by 24 publications

(17 citation statements)

References 51 publications

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“…The 90 kDa heat shock protein (Hsp90) that is involved in modulating oxidative stress in cells [131] can increase Akt activity through the inhibition of inhibiting protein phosphatase 2A (PP2A). In addition, the T cell leukemia/lymphoma 1 (TCL1) protein binds to the PH domain of Akt to increase Akt activity (Figure 1).…”

Section: Signal Transduction and Cell Survival With Pi 3-k Akt Amentioning

confidence: 99%

Oxidant Stress and Signal Transduction in the Nervous System with the PI 3-K, Akt, and mTOR Cascade

Maiese

Chong

Wang

et al. 2012

IJMS

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Oxidative stress impacts multiple systems of the body and can lead to some of the most devastating consequences in the nervous system especially during aging. Both acute and chronic neurodegenerative disorders such as diabetes mellitus, cerebral ischemia, trauma, Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and tuberous sclerosis through programmed cell death pathways of apoptosis and autophagy can be the result of oxidant stress. Novel therapeutic avenues that focus upon the phosphoinositide 3-kinase (PI 3-K), Akt (protein kinase B), and the mammalian target of rapamycin (mTOR) cascade and related pathways offer exciting prospects to address the onset and potential reversal of neurodegenerative disorders. Effective clinical translation of these pathways into robust therapeutic strategies requires intimate knowledge of the complexity of these pathways and the ability of this cascade to influence biological outcome that can vary among disorders of the nervous system.

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Section: Signal Transduction and Cell Survival With Pi 3-k Akt Amentioning

confidence: 99%

Oxidant Stress and Signal Transduction in the Nervous System with the PI 3-K, Akt, and mTOR Cascade

Maiese

Chong

Wang

et al. 2012

IJMS

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“…EPO also can promote bone formation in spinal fusion models [65], modulate vascular dilatation [66], may reduce cerebral aneurysm formation [67] and prevent endothelial cell injury [25–76], protect non-neuronal cells [37,77–80], block disability during infection [28,29,46,81], limit β-amyloid (Aβ) degeneration [26,79,82,83], and may foster memory function [26]. In related systems that directly affect central nervous system function such as the cardiac system, EPO can prevent cardiac injury during chemotherapy [84], improve cardiac contractile function [85], limit cardiac failure through the reduction of inflammation, fibrosis, and oxidative stress [86], and reduce nitrosative stress [87]. These benefits of EPO in the cardiovascular system should correlate with improved cerebral perfusion during cardiac injury.…”

Section: Epo and Cytoprotection In The Nervous Systemmentioning

confidence: 99%

“…EPO can control mitochondrial signaling through Bad, Bax, Puma [27,55,58,76,79,84,91]. EPO also blocks Apaf-1 activation [25,78] and prevents the early activation of several caspases such as caspase 1, caspase 3, and caspase 9 [25,27,44,55,57,59,72,79,87,169,170]. …”

Section: Epo Oxidative Stress and Apoptosismentioning

confidence: 99%

Erythropoietin: New Directions for the Nervous System

Maiese

Chong

Shang

et al. 2012

IJMS

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New treatment strategies with erythropoietin (EPO) offer exciting opportunities to prevent the onset and progression of neurodegenerative disorders that currently lack effective therapy and can progress to devastating disability in patients. EPO and its receptor are present in multiple systems of the body and can impact disease progression in the nervous, vascular, and immune systems that ultimately affect disorders such as Alzheimer’s disease, Parkinson’s disease, retinal injury, stroke, and demyelinating disease. EPO relies upon wingless signaling with Wnt1 and an intimate relationship with the pathways of phosphoinositide 3-kinase (PI 3-K), protein kinase B (Akt), and mammalian target of rapamycin (mTOR). Modulation of these pathways by EPO can govern the apoptotic cascade to control β-catenin, glycogen synthase kinase-3β, mitochondrial permeability, cytochrome c release, and caspase activation. Yet, EPO and each of these downstream pathways require precise biological modulation to avert complications associated with the vascular system, tumorigenesis, and progression of nervous system disorders. Further understanding of the intimate and complex relationship of EPO and the signaling pathways of Wnt, PI 3-K, Akt, and mTOR are critical for the effective clinical translation of these cell pathways into robust treatments for neurodegenerative disorders.

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“…In contrast, the T cell leukemia/lymphoma 1 (TCL1) protein binds to the PH domain of Akt to enhance Akt activity. A 90 kDa heat shock protein (Hsp90) that is involved in modulating oxidative stress in cells [51] also can enhance Akt activity through the inhibition of inhibiting protein phosphatase 2A (PP2A).…”

Section: Cellular Signaling In the Pi 3-k/akt/mtor Cascadementioning

confidence: 99%

A Critical Kinase Cascade In Neurological Disorders: Pi3K, Akt and Mtor

Chong¹,

Shang²,

Wang³

et al. 2012

Future Neurol.

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Neurodegenerative disorders lead to disability and death in a significant proportion of the world’s population. However, many disorders of the nervous system remain with limited effective treatments. Kinase pathways in the nervous system that involve phosphoinositide 3-kinase (PI 3-K), protein kinase B (Akt), and the mammalian target of rapamycin (mTOR) offer exciting prospects for the understanding of neurodegenerative pathways and the development of new avenues of treatment. PI 3-K, Akt, and mTOR pathways are vital cellular components that determine cell fate during acute and chronic disorders, such as Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, epilepsy, stroke, and trauma. Yet, the elaborate relationship among these kinases and the variable control of apoptosis and autophagy can lead to unanticipated biological and clinical outcomes. Crucial for the successful translation of PI 3-K, Akt, and mTOR into robust and safe clinical strategies will be the further elucidation of the complex roles that these kinase pathways hold in the nervous system.

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Erythropoietin alleviates post-ischemic injury of rat hearts by attenuating nitrosative stress

Cited by 24 publications

References 51 publications

Oxidant Stress and Signal Transduction in the Nervous System with the PI 3-K, Akt, and mTOR Cascade

Oxidant Stress and Signal Transduction in the Nervous System with the PI 3-K, Akt, and mTOR Cascade

Erythropoietin: New Directions for the Nervous System

A Critical Kinase Cascade In Neurological Disorders: Pi3K, Akt and Mtor

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