ArticleMolecular biology reports2026
AAV-mediated surtuin 1 overexpression in the cochlear inner hair cells protects ribbon synapses of D-galactose-induced aging mice.
Article in Molecular biology reports, 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
backgroundMitochondrial dysfunction is considered one of the molecular mechanisms underlying age-related hearing loss (ARHL). While some studies have suggested that surtuin 1 (SIRT1) may improve mitochondrial function, delaying the onset of ARHL; other research has indicated that SIRT1 can exacerbate hair cell damage, leading to further hearing loss. We aimed to investigate the role of SIRT1 in ARHL and its associated molecular mechanisms.
methodsEight-week-old male C57BL/6J mice were randomly divided into three groups: control, D-galactose (D-gal), and D-gal+SIRT1. Auditory brainstem response (ABR) was tested to evaluate hearing function. Immunofluorescence (IF) staining was used to assess the number of ribbon synapses. The enzymatic chemistry was applied for measuring reactive oxygen species (ROS) production, and mitochondrial DNA (mtDNA) damage was assessed with RT-PCR. Additionally, western blot (WB) was used to detect SIRT1 protein levels.
resultsCompared with the control group, the D-gal group exhibited elevated ABR thresholds and decreased ABR I wave amplitude, as well as prolonged latency. The results also revealed a decrease in the number of ribbon synapses and increased ROS levels in the D-gal group, as well as decreased SIRT1 protein. SIRT1 overexpression mitigated hearing loss in D-gal-induced accelerated aging mice, with increased ABR I wave amplitude and shorter latency. WB analysis revealed that SIRT1 overexpression reduced total protein acetylation levels. Furthermore, SIRT1 overexpression decreased ROS production, mitigated mtDNA damage and significantly increased the number of synapses.
conclusionsThese findings demonstrate that SIRT1 overexpression suppresses oxidative stress in ARHL, thereby mitigating damage to inner hair cell ribbons and delaying the hearing deterioration in ARHL.
Indexed as
Identifiers
41860621What Socratic 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 Socratic graph.