The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Mechanisms of sensorineural cell damage, death and survival in the cochlea
Open accessAbstract
The majority of acquired hearing loss, including presbycusis, is caused by irreversible damage to the sensorineural tissues of the cochlea. This article reviews the intracellular mechanisms that contribute to sensorineural damage in the cochlea, as well as the survival signaling pathways that can provide endogenous protection and tissue rescue. These data have primarily been generated in hearing loss not directly related to age. However, there is evidence that similar mechanisms operate in presbycusis. Moreover, accumulation of damage from other causes can contribute to age-related hearing loss (ARHL). Potential therapeutic interventions to balance opposing but interconnected cell damage and survival pathways, such as antioxidants, anti-apoptotics, and pro-inflammatory cytokine inhibitors, are also discussed.
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Cites
Correspondence - Tranexamic acid for traumatic brain injury
(2005) · London School of Economics and Political Science Theses Online (London School of Economics and Political Science) · doi:10.1016/s0140-6736 · Cited by 11,894
Chronic Inflammation (Inflammaging) and Its Potential Contribution to Age-Associated Diseases
Franceschi, C., & Campisi, J. (2014) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/glu057 · Cited by 3,891
Adenosine Receptors as Therapeutic Targets
Jacobson, K. A., & Gao, Z.-G. (2006) · Nature Reviews Drug Discovery · doi:10.1038/nrd1983 · Cited by 1,431 · cited 2×
“Adenosine is released from tissue in response to stress as a cytoprotectant, augments antioxidant defense, increases oxygen supply, improves blood flow, inhibits the release of neurotransmitters, stabilizes cells by stimulating K channels and inhibiting Ca2+ channels, triggers antiinflammatory responses, and promotes…”
Background(2014) · doi:10.1523/jneurosci · Cited by 715
Delayed production of free radicals following noise exposure
Yamashita, D., Jiang, H.-Y., Schacht, J., & Miller, J. M. (2004) · Brain Research · doi:10.1016/j.brainres.2004.05.104 · Cited by 352
Cited by
Bowl, M. R., & Dawson, S. J. (2019) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a033217 · Cited by 396
Unmyelinated type II afferent neurons report cochlear damage
Liu, C., Glowatzki, E., & Fuchs, P. A. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1515228112 · Cited by 156
Hearing Outcome of Low-tone Compared to High-tone Sudden Sensorineural Hearing Loss
Psillas, G., Rizou, A., Rachovitsas, D., Tsiropoulos, G., & Constantinidis, J. (2019) · International Archives of Otorhinolaryngology · doi:10.1055/s-0038-1657789 · Cited by 25
Audiological Patterns in Patients with Autoimmune Hearing Loss
Psillas, G., Dimas, G. G., Daniilidis, M., Binos, P., Tegos, T., & Constantinidis, J. (2022) · Audiology and Neurotology · doi:10.1159/000518694 · Cited by 10
Damage-evoked signals in cochlear neurons and supporting cells
Wood, M. B., Nowak, N., & Fuchs, P. A. (2024) · Frontiers in Neurology · doi:10.3389/fneur.2024.1361747 · Cited by 7
“These and stress-activated protein kinases (JNK and P38) have been implicated in the cochlear response to damage (52).”
Background
Metadata
- Authors
- Wong, A. C. Y., & Ryan, A. F.
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2015-04-21
- Volume
- 7
- Pages
- 58-58
- ISSN
- 1663-4365 (ISSN-L)
- OpenAlex
- W2046124242
- Cited by
- 282
- References
- 5
- FWCI
- 16.56
- Type
- journal article
- Language
- en
- Open access
- gold
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