The Role and Mechanism of GSDME-Dependent Pyroptosis in Cochlear Marginal Cells Injury by Cisplatin

<b>Background:</b> Elucidating the mechanisms underlying cisplatin-induced ototoxicity is critical for the clinical management of hearing loss. While cisplatin is known to penetrate the inner ear via the blood-labyrinth barrier in the stria vascularis, its precise damaging effects on mar...

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Main Authors: Wenyang Lei, Wenting Yu, Ting Li, Wei Tang, Shimin Zong, Hongjun Xiao
Format: Article
Language:English
Published: MDPI AG 2025-07-01
Series:Biomedicines
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Online Access:https://www.mdpi.com/2227-9059/13/7/1680
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Summary:<b>Background:</b> Elucidating the mechanisms underlying cisplatin-induced ototoxicity is critical for the clinical management of hearing loss. While cisplatin is known to penetrate the inner ear via the blood-labyrinth barrier in the stria vascularis, its precise damaging effects on marginal cells (MCs) and subsequent hearing impairment remain incompletely understood. Pyroptosis, a gasdermin-mediated inflammatory cell death pathway, may play a key role. This study investigated the involvement of gasdermin E (GSDME)-dependent pyroptosis in cisplatin-induced injury to MCs. <b>Methods:</b> An in vitro cisplatin-induced pyroptosis model was established in MCs. GSDME expression was downregulated using small interfering RNA (siRNA), and caspase-3 activity was inhibited pharmacologically. The critical threshold for pyroptosis induction was determined to be 5 μmol/L cisplatin exposure for 24 h, which activated the caspase-3/GSDME signaling pathway. <b>Results:</b> Cisplatin treatment upregulated GSDME and caspase-3 expression in MCs. Both inhibition of GSDME and pharmacological blockade of caspase-3 significantly attenuated cisplatin-induced cellular damage. Notably, caspase-3 suppression reduced GSDME expression, suggesting a positive regulatory relationship between these mediators. <b>Conclusions:</b> GSDME-mediated pyroptosis plays a pivotal role in cisplatin-induced marginal cell injury, with caspase-3 acting as an upstream regulator of GSDME expression. These findings provide a mechanistic foundation for developing novel therapeutic strategies against cisplatin ototoxicity.
ISSN:2227-9059