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Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress

  • Authors:
    • Zhiqiang Huo
    • Jun Gu
    • Teng He
  • View Affiliations / Copyright

    Affiliations: Department of Otolaryngology, Affiliated Changshu Hospital of Nantong University, Changshu, Jiangsu 215500, P.R. China
    Copyright: © Huo et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 226
    |
    Published online on: March 26, 2024
       https://doi.org/10.3892/etm.2024.12515
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Abstract

The complex manifestation of diabetic hearing loss and the relative inaccessibility of the inner ear contribute to the lack of research. The present study aimed to reveal the role of Apelin‑13, a critical regulator of lipid metabolism, in diabetes‑induced hearing loss. Cochlear hair cells treated with high glucose (HG) were adopted as an in vitro research model, and the impacts of Apelin‑13 on cellular oxidative stress, apoptosis, mitochondrial dysfunction and endoplasmic reticulum (ER) stress were determined. In addition, cells were treated with the ER stress agonist tunicamycin to further explore its potential role in the regulatory effects of Apelin‑13. Apelin‑13 inhibited oxidative stress and apoptosis in the HG‑induced cells. Additionally, Apelin‑13 elevated mitochondrial membrane potential and ATP production, whereas it reduced mitochondrial reactive oxygen species levels. The levels of ER stress‑related proteins exhibited a downward trend in response to Apelin‑13. By contrast, tunicamycin reversed the effects of Apelin‑13 on the aforementioned aspects, suggesting the role of ER stress in the regulatory effects of Apelin‑13. In conclusion, the present study elucidated the protective role of Apelin‑13 in ameliorating HG‑induced mitochondrial functional impairment in cochlear hair cells by inhibiting ER stress.
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Copy and paste a formatted citation
Spandidos Publications style
Huo Z, Gu J and He T: Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress. Exp Ther Med 27: 226, 2024.
APA
Huo, Z., Gu, J., & He, T. (2024). Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress. Experimental and Therapeutic Medicine, 27, 226. https://doi.org/10.3892/etm.2024.12515
MLA
Huo, Z., Gu, J., He, T."Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress". Experimental and Therapeutic Medicine 27.5 (2024): 226.
Chicago
Huo, Z., Gu, J., He, T."Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress". Experimental and Therapeutic Medicine 27, no. 5 (2024): 226. https://doi.org/10.3892/etm.2024.12515
Copy and paste a formatted citation
x
Spandidos Publications style
Huo Z, Gu J and He T: Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress. Exp Ther Med 27: 226, 2024.
APA
Huo, Z., Gu, J., & He, T. (2024). Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress. Experimental and Therapeutic Medicine, 27, 226. https://doi.org/10.3892/etm.2024.12515
MLA
Huo, Z., Gu, J., He, T."Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress". Experimental and Therapeutic Medicine 27.5 (2024): 226.
Chicago
Huo, Z., Gu, J., He, T."Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress". Experimental and Therapeutic Medicine 27, no. 5 (2024): 226. https://doi.org/10.3892/etm.2024.12515
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