ArticleMolecular medicine reports2015
NADPH oxidase 3‑associated oxidative stress and caspase 3‑dependent apoptosis in the cochleae of D‑galactose‑induced aged rats.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers, 1 of them a synthesis that pooled it.
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.
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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
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Correlation between mitochondrial DNA 4977 bp deletion and presbycusis: A system review and meta-analysis.Medicine · 2019Pooled it
- NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024Review
- Article
- Loss of vacuolar-type H+-ATPase induces caspase-independent necrosis-like death of hair cells in zebrafish neuromasts.Disease models & mechanisms · 2021Article
- Protective Effects of Silymarin Against Age-Related Hearing Loss in an Aging Rat Model.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2019Article
- Leonurine ameliorates D-galactose-induced aging in mice through activation of the Nrf2 signalling pathway.Aging · 2019Article
- Actinidia chinensis planch polysaccharide protects against hypoxia‑induced apoptosis of cardiomyocytes in vitro.Molecular medicine reports · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative damage to mitochondrial DNA (mtDNA) and cell apoptosis are heavily implicated in aging. Our previous study established a mimetic rat model of aging in the cochleae using D‑galactose (D‑gal), and revealed that chronic injection of D‑gal can increase oxidative stress and mtDNA common deletions (CD). The aim of the present study was to investigate the sources of reactive oxygen species and the occurrence of apoptosis in the cochleae of rats following 8 weeks of D‑gal exposure. The results of the present study indicated that an elevated accumulation of the mtDNA CD and mitochondrial ultrastructural damage occurred in the cochleae of rats injected with D‑gal for 8 weeks. In addition, the levels of 8‑hydroxy‑2‑deoxyguanosine, NADPH oxidase (NOX) 3, P22phox and cleaved caspase 3, and the number of terminal deoxynucleotidyl transferase‑mediated deoxyuridine triphosphate nick‑end‑labelling‑positive cells were increased in the cochleae of D‑gal‑treated rats, compared with the controls. These findings suggested that nitric oxide synthase NOX3‑associated oxidative stress may contribute to the accumulation of mtDNA mutations and activate a caspase 3‑dependent apoptotic signalling pathway in the cochleae during aging. The present study also provided novel insights into the development of age‑associated hearing loss, also termed presbycusis.
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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.