ArticleCureus2025
Mitochondrial Hearing Loss: Genetic Variants and Clinical Progression.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Systematic Engineering of Loss-of-Function Alleles in the Zebrafish Mitochondrial Proteome.bioRxiv : the preprint server for biology · 2026Article
- Genetic and Environmental Factors Shaping Hearing Loss: Xenobiotics, Mechanisms and Translational Perspectives.Journal of xenobiotics · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial diseases can affect multiple organ systems including the auditory pathway, leading to sensorineural hearing loss (SNHL). Although several mitochondrial DNA (mtDNA) mutations are linked to progressive hearing impairment, the underlying mechanisms and clinical course of mitochondrial hearing loss remain incompletely understood. In the present study, we analyzed the frequency and progression of mitochondrial mutations in 15 patients diagnosed with unexplained SNHL who underwent genetic testing at our institution. The most common mutations were m.3243A>G and m.1555A>G. Both are of particular interest due to their relatively high prevalence among mitochondrial mutations and strong clinical implications-m.3243A>G is linked to mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) and diabetes, while m.1555A>G is associated with aminoglycoside-induced and non-syndromic hearing loss. Hearing loss associated with m.3243A>G is generally progressive, although the rate of deterioration varies among individuals. In contrast, the m.1555A>G cases remained stable throughout the follow-up period. No significant correlation was observed between the heteroplasmy levels and hearing deterioration, although a weak negative association was observed. Despite significant hearing impairment, hearing aids are underutilized by a considerable proportion of patients. These findings provide new insights into the phenotypic variability of mitochondrial hearing loss and underscore the need for longitudinal studies to assess its natural progression and potential therapeutic interventions.
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Registered trials
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