ArticleOtolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery2026
CSNK1A1 Mediates Inner Ear Inflammation and Endolymphatic Hydrops in a Lipopolysaccharide-Induced Mouse Model.
Article in Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
objectiveOur previous studies demonstrated that casein kinase 1α1 (CSNK1A1) was significantly upregulated in the endolymphatic sac of patients with Meniere's disease (MD). However, its specific role in the development of MD remains unclear. This study aims to investigate the effects of CSNK1A1 inhibition on alleviating hydrops, inflammation, and preserving audiovestibular function in a mouse model of endolymphatic hydrops (EH). STUDY
designExperimental animal study.
settingTranslational research laboratory.
methodsAn EH model was induced in mice by postauricular lipopolysaccharide (LPS) injection. CSNK1A1 localization in hair cells was visualized via immunofluorescence. To functionally interrogate CSNK1A1, mice received intraperitoneal injections of the CSNK1A1 inhibitor CSNK1-IN-2. Evaluations encompassed three key parameters: cochlear morphology (EH severity), auditory brainstem response (ABR) and vestibular evoked myogenic potential (VEMP, audiovestibular function), and immunofluorescence for CD45 and F4/80 (macrophage infiltration).
resultsIn LPS-induced EH mice, CSNK1A1 expression was significantly upregulated in cochlear and vestibular hair cells. Pharmacological inhibition of CSNK1A1 markedly improved audiovestibular function, reducing ABR thresholds (all frequencies, P < .01) and attenuating VEMP latency prolongations (P < .0001), CSNK1A1 inhibition also reduced EH, decreasing the membrane length increase rate (P < .01), and decreased the infiltration of CD45
conclusionCSNK1A1 plays a role in attenuating LPS-induced inner ear injury, suggesting that its inhibition may represent a potential strategy for attenuating inflammation-associated cochleovestibular damage.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.