Cisplatin cytotoxicity of auditory cells requires secretions of proinflammatory cytokines via activation of ERK and NF-kappaB. - Wikidata - wikimedia - TriplyDB

Cisplatin cytotoxicity of auditory cells requires secretions of proinflammatory cytokines via activation of ERK and NF-kappaB.

Cisplatin cytotoxicity of auditory cells requires secretions of proinflammatory cytokines via activation of ERK and NF-kappaB.

http://www.wikidata.org/entity/Q36881759

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Cisplatin ototoxicity and protection: clinical and experimental studies Conservation of hearing and protection of hair cells in cochlear implant patients' with residual hearing Involvement of Ubiquitin-Editing Protein A20 in Modulating Inflammation in Rat Cochlea Associated with Silver Nanoparticle-Induced CD68 Upregulation and TLR4 Activation An integrated view of cisplatin-induced nephrotoxicity and ototoxicity Changes in Gene Expression and Hearing Thresholds After Cochlear Implantation.Association between polymorphism of interleukin-6 in the region -174G/C and tinnitus in the elderly with a history of occupational noise exposure.IL-10/HMOX1 signaling modulates cochlear inflammation via negative regulation of MCP-1/CCL2 expression in cochlear fibrocytes.Heat shock protein-mediated protection against Cisplatin-induced hair cell death.Loss of STAT1 protects hair cells from ototoxicity through modulation of STAT3, c-Jun, Akt, and autophagy factors.Cisplatin exposure damages resident stem cells of the mammalian inner ear.Tumor Necrosis Factor-α-Induced Ototoxicity in Mouse Cochlear Organotypic Culture.Molecular regulation of auditory hair cell death and approaches to protect sensory receptor cells and/or stimulate repair following acoustic trauma.Tumor necrosis factor-alpha-mutant mice exhibit high frequency hearing loss.Cisplatin ototoxicity blocks sensory regeneration in the avian inner ear Receptor-interacting protein kinases modulate noise-induced sensory hair cell death Efficacy of three drugs for protecting against gentamicin-induced hair cell and hearing losses.The design and screening of drugs to prevent acquired sensorineural hearing loss Short interfering RNA against STAT1 attenuates cisplatin-induced ototoxicity in the rat by suppressing inflammation Augmentation of NAD(+) by NQO1 attenuates cisplatin-mediated hearing impairment.Late-onset Mitochondrial Cardiomyopathy Triggered by Anticancer Treatment Systemic dexamethasone for the prevention of cisplatin-induced ototoxicity.Cisplatin ototoxicity involves cytokines and STAT6 signaling network.Mechanism of Cisplatin-Induced Cytotoxicity Is Correlated to Impaired Metabolism Due to Mitochondrial ROS Generation.Pre-conditioning with near infrared photobiomodulation reduces inflammatory cytokines and markers of oxidative stress in cochlear hair cells.Extracellular signal-regulated kinases modulate DNA damage response - a contributing factor to using MEK inhibitors in cancer therapy.The impact of erdosteine on cisplatin-induced ototoxicity: a proteomics approach.Increased risk of sudden sensorineural hearing loss in patients with hepatitis virus infection.Adenosine A1 Receptor Protects Against Cisplatin Ototoxicity by Suppressing the NOX3/STAT1 Inflammatory Pathway in the Cochlea.Evidence that cisplatin-induced auditory damage is attenuated by downregulation of pro-inflammatory cytokines via Nrf2/HO-1 Proteomic analysis of the balance between survival and cell death responses in cisplatin-mediated ototoxicity.A combination of cilostazol and Ginkgo biloba extract protects against cisplatin-induced Cochleo-vestibular dysfunction by inhibiting the mitochondrial apoptotic and ERK pathways.Cisplatin-induced hair cell death requires STAT1 and is attenuated by epigallocatechin gallate.NAD(+) Metabolism in Age-Related Hearing Loss Capsaicin ameliorates cisplatin-induced renal injury through induction of heme oxygenase-1.Reactive oxygen species in apoptosis induced by cisplatin: review of physiopathological mechanisms in animal models.Molecular and cellular mechanisms of loss of residual hearing after cochlear implantation.Signalling mechanisms involved in renal pathological changes during cisplatin-induced nephropathy.Prophylactic etanercept treatment in cisplatin ototoxicity.3-Aminotriazole protects from CoCl2-induced ototoxicity by inhibiting the generation of reactive oxygen species and proinflammatory cytokines in mice.Protective effect of acetyl-l-carnitine against cisplatin ototoxicity: role of apoptosis-related genes and pro-inflammatory cytokines.

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Cisplatin cytotoxicity of auditory cells requires secretions of proinflammatory cytokines via activation of ERK and NF-kappaB.

http://www.wikidata.org/entity/Q36881759

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Cisplatin cytotoxicity of audi ...... tivation of ERK and NF-kappaB.

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David J Lim

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Eunsook Kim

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Haa-Yung Lee

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Hongseob So

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HyungJin Kim

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Jin-Kyung Kim

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Kang-Min Lee

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Ki-Jung Yun

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Raekil Park

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P2860

The NF-kappa B and I kappa B proteins: new discoveries and insights

NF-kappa B and Rel proteins: evolutionarily conserved mediators of immune responses

Gap junctions in the rat cochlea: immunohistochemical and ultrastructural analysis

Lipopolysaccharide activation of the MEK-ERK1/2 pathway in human monocytic cells mediates tissue factor and tumor necrosis factor alpha expression by inducing Elk-1 phosphorylation and Egr-1 expression

Free radicals and hearing. Cause, consequence, and criteria

Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases

Mitogen-activated protein kinase: conservation of a three-kinase module from yeast to human

Reactive oxygen species and proinflammatory cytokine signaling in endothelial cells: effect of selenium supplementation.

Cisplatin-induced apoptotic cell death in Mongolian gerbil cochlea.

Application of antioxidants and other agents to prevent cisplatin ototoxicity.

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