Celecoxib-Dependent Neuroprotection in a Rat Model of Transient Middle Cerebral Artery Occlusion (tMCAO) Involves Modifications in Unfolded Protein Response (UPR) and Proteasome

Santos‐Galdiano, María; González‐Rodríguez, Paloma; Font‐Belmonte, Enrique; Ugidos, Irene F; Anuncibay‐Soto, Berta; Pérez‐Rodríguez, Diego; Fernández‐López, Arsenio

doi:10.1007/s12035-020-02202-y

Cited by 7 publications

(2 citation statements)

References 70 publications

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“…Regarding UPR activation, celecoxib reduces ERS by promoting the IRE1-UPR pathway and ultimately exerts a neuroprotective effect ( Santos-Galdiano et al, 2021 ). In addition, IRE1 contributes to ERS-mediated apoptosis through the c-Jun N-terminal kinase (JNK) and caspase-12 pathways.…”

Section: Signal Transduction Pathways Involved In Endoplasmic Reticul...mentioning

confidence: 99%

Endoplasmic Reticulum Stress and the Unfolded Protein Response in Cerebral Ischemia/Reperfusion Injury

Wang

Liu

Zhou

et al. 2022

Front. Cell. Neurosci.

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Ischemic stroke is an acute cerebrovascular disease characterized by sudden interruption of blood flow in a certain part of the brain, leading to serious disability and death. At present, treatment methods for ischemic stroke are limited to thrombolysis or thrombus removal, but the treatment window is very narrow. However, recovery of cerebral blood circulation further causes cerebral ischemia/reperfusion injury (CIRI). The endoplasmic reticulum (ER) plays an important role in protein secretion, membrane protein folding, transportation, and maintenance of intracellular calcium homeostasis. Endoplasmic reticulum stress (ERS) plays a crucial role in cerebral ischemia pathophysiology. Mild ERS helps improve cell tolerance and restore cell homeostasis; however, excessive or long-term ERS causes apoptotic pathway activation. Specifically, the protein kinase R-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6), and inositol-requiring enzyme 1 (IRE1) pathways are significantly activated following initiation of the unfolded protein response (UPR). CIRI-induced apoptosis leads to nerve cell death, which ultimately aggravates neurological deficits in patients. Therefore, it is necessary and important to comprehensively explore the mechanism of ERS in CIRI to identify methods for preserving brain cells and neuronal function after ischemia.

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Section: Signal Transduction Pathways Involved In Endoplasmic Reticul...mentioning

confidence: 99%

Endoplasmic Reticulum Stress and the Unfolded Protein Response in Cerebral Ischemia/Reperfusion Injury

Wang

Liu

Zhou

et al. 2022

Front. Cell. Neurosci.

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show abstract

“…Celecoxib is a well-known anti-inflammatory, recently proclaimed to reduce ER stress by decreasing the expression of glucose-related protein 78 (GRP78), CHOP, and caspase-12 after 48 hours of reperfusion. Additionally, celecoxib was also showcased to enhance the IRE1-UPR pathway, further reducing ER stress [ 49 ].…”

Section: Pharmacological Therapiesmentioning

confidence: 99%

Intertwined Relation between the Endoplasmic Reticulum and Mitochondria in Ischemic Stroke

Peng

Ghosh

Pang

et al. 2022

Oxidative Medicine and Cellular Longevity

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In ischemic stroke (IS), accumulation of the misfolded proteins in the endoplasmic reticulum (ER) and mitochondria-induced oxidative stress (OS) has been identified as the indispensable inducers of secondary brain injury. With the increasing recognition of an association between ER stress and OS with ischemic stroke and with the improved understanding of the underlying molecular mechanism, novel targets for drug therapy and new strategies for therapeutic interventions are surfacing. This review discusses the molecular mechanism underlying ER stress and OS response as both causes and consequences of ischemic stroke. We also summarize the latest advances in understanding the importance of ER stress and OS in the pathogenesis of ischemic stroke and discuss potential strategies and clinical trials explicitly aiming to restore mitochondria and ER dynamics after IS.

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Celecoxib attenuates neuroinflammation, reactive astrogliosis and promotes neuroprotection in young rats with experimental hydrocephalus

Dutra,

Covas da Silva,

da Silva Beggiora Marques

et al. 2023

Journal of Chemical Neuroanatomy

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Celecoxib-Dependent Neuroprotection in a Rat Model of Transient Middle Cerebral Artery Occlusion (tMCAO) Involves Modifications in Unfolded Protein Response (UPR) and Proteasome

Cited by 7 publications

References 70 publications

Endoplasmic Reticulum Stress and the Unfolded Protein Response in Cerebral Ischemia/Reperfusion Injury

Endoplasmic Reticulum Stress and the Unfolded Protein Response in Cerebral Ischemia/Reperfusion Injury

Intertwined Relation between the Endoplasmic Reticulum and Mitochondria in Ischemic Stroke

Celecoxib attenuates neuroinflammation, reactive astrogliosis and promotes neuroprotection in young rats with experimental hydrocephalus

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