Related Experiment Video
Updated: May 5, 2026
The Mouse Round-window Approach for Ototoxic Agent Delivery: A Rapid and Reliable Technique for Inducing Cochlear Cell Degeneration
Published on: November 26, 2015
Expression of SLC2A1 is upregulated in a mouse model of age-related hearing loss
Jiali Liu1, Haisen Peng1, Yuehui Liu1
1Department of Otolaryngology, Head and Neck Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, Jiangxi, China.
Background:
Age-related hearing loss (ARHL) is a common issue associated with aging. One of the typical causes of hearing loss is the irreversible death of hair cells. In addition, oxidative stress contributes to ARHL. However, the underlying molecular mechanism in ARHL is not well understood.
Methods:
The ARHL samples were from GSE153882 datasets of the Gene Expression Omnibus database. The Limma R-package was used to identify differentially expressed genes. The hub gene was obtained via intersection of oxidative stress genes and cuproptosis genes. Hearing function was measured using the auditory brainstem response (ABR). Western blot and immunofluorescence were used to examine solute carrier family 2 member 1 protein (SLC2A1), dihydrolipoyl transacetylase (DLAT) an dihydrolipoamide dehydrogenase (DLD) in vitro and in vivo.
Results:
Oxidative stress gene SLC2A1 (also named GLUT1) is related to cuproptosis gene in age-related hearing loss. In the ARHL mice model, SLC2A1, DLAT and DLD were elevated. The ABR recordings showed that SLC2A1 knockdown lowered the average thresholds of mice. Knockdown SLC2A1 alleviated DLAT and DLD in vitro and in vivo.
Conclusion:
Our findings highlight SLC2A1 as an essential driver of cuproptosis and ARHL. Knockdown SLC2A1 suppresses ARHL progression via inhibiting cuproptosis.
