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April 21, 2026Communications BiologyOpen Access

BAX-dependent mitochondrial outer membrane rupture in cochlear hair cells facilitates cisplatin ototoxicity

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Authors

JPJing PanKWKaiye WangJQJiaxi Qu

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Overview

Demonstrates BAX involvement in hearing loss from cisplatin, suggesting a possible treatment route to protect cochlear hair cells.

Key Points

  • To explore the mechanism of cisplatin-induced hearing loss in cochlear hair cells through mitochondrial dysfunction and BAX activity.
  • Used super-resolution and transmission electron microscopy on HEI-OC1 cells and murine cochlear explants.
  • Conducted subcellular fractionation and functional assays to assess mitochondrial integrity and function.
  • Administered BAX inhibitor peptide V5 in vitro and in vivo for protective effects against cisplatin toxicity.
  • Identified BAX translocation and oligomerization as key factors in mitochondrial membrane rupture due to cisplatin.
  • BAX inhibition preserved mitochondrial function, reduced reactive oxygen species, and limited hair cell loss.
  • In vivo treatment with BipV5 decreased outer hair cell loss and provided sustained functional protection.

Cite This Study

Pan et al. (2026) studied this question.

synapsesocial.com/papers/69e7138bcb99343efc98d016https://doi.org/10.1038/s42003-026-10080-8
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