ArticleScientific reports2017
NLRX1 accelerates cisplatin-induced ototoxity in HEI-OC1 cells via promoting generation of ROS and activation of JNK signaling pathway.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Drug Nanocrystal-Loaded Thermo-Reversible Hydrogels of Dexamethasone Palmitate for Intratympanic Drug Delivery.Journal of functional biomaterials · 2026Article
- Repeated air pollution exposure predisposes to adverse outcomes from acute lung injury.Particle and fibre toxicology · 2026Article
- Targeting Autophagy for Otoprotection: Translating Basic Mechanisms into Clinical Strategies.International journal of molecular sciences · 2026Review
- Protective effect of trans-sodium crocetinate on nephrotoxicity induced by cisplatin: in vitro and in vivo models.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- NLRX1 mediated impaired microglial phagocytosis of NETs in cerebral ischemia and reperfusion injury.Cell death and differentiation · 2025Article
- An In Vitro Oxidative Stress Model of the Human Inner Ear Using Human-Induced Pluripotent Stem Cell-Derived Otic Progenitor Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Protection from cisplatin-induced hearing loss with lentiviral vector-mediated ectopic expression of the anti-apoptotic protein BCL-XL.Molecular therapy. Nucleic acids · 2024Article
- Hearing loss during chemotherapy: prevalence, mechanisms, and protection.American journal of cancer research · 2024Review
- Cellular Context Dictates the Suppression or Augmentation of Triple-Negative Mammary Tumor Metastasis by NLRX1.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Lysophosphatidic acid exerts protective effects on HEI-OC1 cells against cytotoxicity of cisplatin by decreasing apoptosis, excessive autophagy, and accumulation of ROS.Cell death discovery · 2023Article
- Apelin-13 protects against cisplatin-induced ototoxicity by inhibiting apoptosis and regulating STAT1 and STAT3.Archives of toxicology · 2023Article
- NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury.Scientific reports · 2023Article
- Sex-Biased Control of Inflammation and Metabolism by a Mitochondrial Nod-Like Receptor.Frontiers in immunology · 2022Article
- Metabolic regulators of enigmatic inflammasomes in autoimmune diseases and crosstalk with innate immune receptors.Immunology · 2021Review
- Focusing on the Cell Type Specific Regulatory Actions of NLRX1.International journal of molecular sciences · 2021Review
- Role of NLRs in the Regulation of Type I Interferon Signaling, Host Defense and Tolerance to Inflammation.International journal of molecular sciences · 2021Review
- Analysis of Factors Affecting Cranial Nerve Function of Patients With Vascular Mild Cognitive Impairment Through Functional Magnetic Resonance Imaging Under Artificial Intelligence Environment.Frontiers in public health · 2021Article
- Autophagy: A Novel Horizon for Hair Cell Protection.Neural plasticity · 2021Review
- Protective Effects of Glucose-Related Protein 78 and 94 on Cisplatin-Mediated Ototoxicity.Antioxidants (Basel, Switzerland) · 2020Article
- Impaired Glycolysis Promotes AlcoholExposure-Induced Apoptosis in HEI-OC1 Cells via Inhibition of EGFR Signaling.International journal of molecular sciences · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide-binding domain and leucine-rich-repeat-containing family member X1 (NLRX1), located in mitochondria, can recognize cytoplasmic pattern recognition receptors and is tightly related to reactive oxygen species (ROS) production, mitochondrial function, apoptosis and inflammation. The present study was designed to explore whether NLRX1 expresses in HEI-OC1 cells and, if so, to investigate the possible correlations between NLRX1 and cisplatin-induced ototoxity in vitro. Here, we report that NLRX1 was specifically localized to mitochondria in the cytoplasm of HEI-OC1 cells and its expression was increased concurrent with the increase of ROS production and occurrence of apoptosis in HEI-OC1 cells in response to cisplatin stimulus. NLRX1 overexpression led to a higher apoptosis in HEI-OC1 cells treated with cisplatin, whereas, NLRX silencing decreased cisplatin induced apoptosis. Mechanistic studies showed that NLRX1 activated mitochondrial apoptosis pathway as well as promoted ROS generation and JNK activation. Either inhibition of ROS generation or JNK signaling significantly prevented NLRX1-mediated mitochondrial apoptosis in HEI-OC1cells. In addition, NLRX1 expression was confirmed in cochlear explants. The findings from this work reveal that NLRX1 sensitizes HEI-OC1 cells to cisplatin-induced apoptosis via activation of ROS/JNK signaling pathway, suggesting that NLRX1 acts as an important regulator of the cisplatin-elicited ototoxity.
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