Activation of NLRX1-mediated autophagy accelerates the ototoxic potential of cisplatin in auditory cells

Yin, Haiyan; Yang, Qianqian; Cao, Zhixin; Li, Hongrui; Yu, Zhaoyan; Zhang, Guodong; Sun, Gaoying; Man, Rongjun; Wang, Haibo; Li, Jianfeng

doi:10.1016/j.taap.2018.02.007

Cited by 31 publications

(21 citation statements)

References 49 publications

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“…NLRX1 overexpression led to the amount of accumulation of autophagosomes in HEI‐OC1 cells in normal condition and a higher activation of autophagy concurrent with cell injury in HEI‐OC1 cells treated with cisplatin. These findings suggest that decrease the activation level of autophagy concurrent with increased cell viability in HEI‐OC1 cells treated with cisplatin, while overactivation of autophagy can lead to pathological changes in response to cisplatin exposure 12 . MicroRNA‐96 is the first microRNA mutation that has been reported to be related to human deafness 149 .…”

Section: Autophagic Pathways In Hlmentioning

confidence: 93%

“…Yin et al found that autophagic activation of HEI‐OC1 cells increased the expression of the nuclear binding domain and leucine‐rich repeat containing family member X1 (NLRX1) in cisplatin‐induced injury 12 . NLRX1 overexpression led to the amount of accumulation of autophagosomes in HEI‐OC1 cells in normal condition and a higher activation of autophagy concurrent with cell injury in HEI‐OC1 cells treated with cisplatin.…”

Section: Autophagic Pathways In Hlmentioning

confidence: 99%

“…It is a key mechanism in the response of cells to extracellular or intracellular stress that aid in their survival under certain circumstances; for instance, autophagy protects cells against NIHL by attenuating oxidative stress 11 . However, overactivation of autophagy may result in cell death 12 . Specialized double‐membrane vesicles, known as autophagosomes, encapsulate degenerating cytoplasmic organelles or cytosol and subsequently degrade them via the fusion with lysosomes 13,14 .…”

Section: Introductionmentioning

confidence: 99%

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Programmed cell death pathways in hearing loss: A review of apoptosis, autophagy and programmed necrosis

Kong

et al. 2020

Cell Proliferation

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Programmed cell death (PCD)—apoptosis, autophagy and programmed necrosis—is any pathological form of cell death mediated by intracellular processes. Ototoxic drugs, ageing and noise exposure are some common pathogenic factors of sensorineural hearing loss (SNHL) that can induce the programmed death of auditory hair cells through different pathways, and eventually lead to the loss of hair cells. Furthermore, several mutations in apoptotic genes including DFNA5, DFNA51 and DFNB74 have been suggested to be responsible for the new functional classes of monogenic hearing loss (HL). Therefore, in this review, we elucidate the role of these three forms of PCD in different types of HL and discuss their guiding significance for HL treatment. We believe that further studies of PCD pathways are necessary to understand the pathogenesis of HL and guide scientists and clinicians to identify new drug targets for HL treatment.

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Section: Autophagic Pathways In Hlmentioning

confidence: 93%

Section: Autophagic Pathways In Hlmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Programmed cell death pathways in hearing loss: A review of apoptosis, autophagy and programmed necrosis

Kong

et al. 2020

Cell Proliferation

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“…Both activation and inhibition of autophagy can reduce cisplatin-induced ototoxicity. For example, inhibition of ROS generation significantly prevents autophagy activation and apoptosis in response to cisplatin exposure ( Yin et al., 2018 ). Further, enhancing autophagy can alleviate cisplatin-induced ototoxicity in rats ( Liu et al., 2019 ) and zebrafish ( Pang et al., 2018 ).…”

Section: Mechanisms Of Cisplatin-induced Ototoxicitymentioning

confidence: 99%

Current Strategies to Combat Cisplatin-Induced Ototoxicity

Chen

et al. 2020

Front. Pharmacol.

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Cisplatin is widely used for the treatment of a number of solid malignant tumors. However, ototoxicity induced by cisplatin is an obstacle to effective treatment of tumors. The basis for this toxicity has not been fully elucidated. It is generally accepted that hearing loss is due to excessive production of reactive oxygen species by cells of the cochlea. In addition, recent data suggest that inflammation may trigger inner ear cell death through endoplasmic reticulum stress, autophagy, and necroptosis, which induce apoptosis. Strategies have been extensively explored by which to prevent, alleviate, and treat cisplatin-induced ototoxicity, which minimize interference with antitumor activity. Of these strategies, none have been approved by the Federal Drug Administration, although several preclinical studies have been promising. This review highlights recent strategies that reduce cisplatin-induced ototoxicity. The focus of this review is to identify candidate agents as novel molecular targets, drug administration routes, delivery systems, and dosage schedules. Animal models of cisplatin ototoxicity are described that have been used to evaluate drug efficacy and side effect prevention. Finally, clinical reports of otoprotection in patients treated with cisplatin are highlighted. For the future, high-quality studies are required to provide reliable data regarding the safety and effectiveness of pharmacological interventions that reduce cisplatin-induced ototoxicity.

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“…При использовании аудиометрии с расширенным диапазоном частот ототоксичность диагностируется практически у всех пациентов, получающих цисплатин, однако клинически это может не проявляться, так как «выпадающие» высокие частоты находятся вне речевого диапазона [37].…”

Section: ототоксичностьunclassified

Late complications of the treatment of patients with germ cell tumors

et al. 2020

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Germ cell tumors are one of the highly sensitive to chemotherapy, and about 80 % of patients can be cured even having metastases. Apartfrom acute toxicity, chemotherapy is characterized by late complications that occur many years later and not only negatively affect the quality of life, but in some cases are life-threatening. The review summarizes the results of studies on the late complications’ occurrence and prevention when treating patients with germ cell tumors.

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Activation of NLRX1-mediated autophagy accelerates the ototoxic potential of cisplatin in auditory cells

Cited by 31 publications

References 49 publications

Programmed cell death pathways in hearing loss: A review of apoptosis, autophagy and programmed necrosis

Programmed cell death pathways in hearing loss: A review of apoptosis, autophagy and programmed necrosis

Current Strategies to Combat Cisplatin-Induced Ototoxicity

Late complications of the treatment of patients with germ cell tumors

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