ArticleThe Journal of clinical investigation2025
A deafness-blindness syndrome results from ATF6-based disruption of the unfolded protein response.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Subtype-Specific Vulnerability of Spiral Ganglion Neurons in Sensorineural Hearing Loss Across the Lifespan.Brain sciences · 2026Review
- Heat-shock pathway activation by TRC051384 protects spiral ganglion neurons from noise-induced hearing loss.bioRxiv : the preprint server for biology · 2025Article
- Folic acid prevents inner hair cell degeneration via genomic stability.Cell death discovery · 2025Article
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Authors and funding
2 authors.
Funding
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Abstract
Sensorineural hearing loss (SNHL) is the most prevalent form of permanent hearing impairment, arising from factors such as aging, exposure to loud noise, disease, ototoxic medications, and genetic mutations. Despite extensive research, effective treatments or cures for SNHL remain elusive. In this issue of the JCI, Lee et al. reveal a link between mutations in ATF6 and SNHL in patients with achromatopsia. The study also shows that Atf6-deficient (Atf6-/-) mice exhibit disorganized stereocilia and age-related loss of outer hair cells. Additionally, the researchers show that Atf6 is critical for cochlear hair cell function. Mice lacking Atf6 expression experienced ER stress, which ultimately led to SNHL. Collectively, these findings enhance our understanding of the emerging role of protein homeostasis and ER stress in the pathogenesis of SNHL.
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