ArticleScientific reports2016
The redox protein p66(shc) mediates cochlear vascular dysfunction and transient noise-induced hearing loss.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Oxidative stress and reactive oxygen species in otorhinolaryngological diseases: insights from pathophysiology to targeted antioxidant therapies.Redox report : communications in free radical research · 2025Review
- Intestinal inflammation and microbiota modulation impact cochlear function: emerging insights in gut-ear axis.Cell communication and signaling : CCS · 2025Article
- Health position paper and redox perspectives - Disease burden by transportation noise.Redox biology · 2024Review
- Oxidative stress and inflammation cause auditory system damage via glial cell activation and dysregulated expression of gap junction proteins in an experimental model of styrene-induced oto/neurotoxicity.Journal of neuroinflammation · 2024Article
- Redox Imbalance as a Common Pathogenic Factor Linking Hearing Loss and Cognitive Decline.Antioxidants (Basel, Switzerland) · 2023Review
- P66Shc is increased in peripheral blood mononuclear cells of the patients with obstructive sleep apnea.International journal of medical sciences · 2023Article
- Early Noise-Induced Hearing Loss Accelerates Presbycusis Altering Aging Processes in the Cochlea.Frontiers in aging neuroscience · 2022Article
- Article
- Transportation noise pollution and cardiovascular disease.Nature reviews. Cardiology · 2021Review
- Intense noise exposure alters peripheral vestibular structures and physiology.Journal of neurophysiology · 2020Article
- Evaluation of Serum Endocan Levels in Sensorineural Hearing Loss.The journal of international advanced otology · 2019Article
- Downregulation of p66Shc can reduce oxidative stress and apoptosis in oxidative stress model of marginal cells of stria vascularis in Sprague Dawley rats.Drug design, development and therapy · 2019Article
- The Adverse Effects of Environmental Noise Exposure on Oxidative Stress and Cardiovascular Risk.Antioxidants & redox signaling · 2018Review
- P66Molecular neurobiology · 2017Review
- NLRP3-inflammasomes are triggered by age-related hearing loss in the inner ear of mice.American journal of translational research · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p66(shc), a member of the ShcA protein family, is essential for cellular response to oxidative stress, and elicits the formation of mitochondrial Reactive Oxygen Species (ROS), thus promoting vasomotor dysfunction and inflammation. Accordingly, mice lacking the p66 isoform display increased resistance to oxidative tissue damage and to cardiovascular disorders. Oxidative stress also contributes to noise-induced hearing loss (NIHL); we found that p66(shc) expression and serine phosphorylation were induced following noise exposure in the rat cochlea, together with markers of oxidative stress, inflammation and ischemia as indicated by the levels of the hypoxic inducible factor (HIF) and the vascular endothelial growth factor (VEGF) in the highly vascularised cochlear lateral region and spiral ganglion. Importantly, p66(shc) knock-out (p66 KO) 126 SvEv adult mice were less vulnerable to acoustic trauma with respect to wild type controls, as shown by preserved auditory function and by remarkably lower levels of oxidative stress and ischemia markers. Of note, decline of auditory function observed in 12 month old WT controls was markedly attenuated in p66KO mice consistent with delayed inner ear senescence. Collectively, we have identified a pivotal role for p66(shc) -induced vascular dysfunction in a common pathogenic cascade shared by noise-induced and age-related hearing loss.
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Registered trials
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