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Review
. 2015 Apr 21:7:58.
doi: 10.3389/fnagi.2015.00058. eCollection 2015.

Mechanisms of sensorineural cell damage, death and survival in the cochlea

Ann C Y Wong  1 , Allen F Ryan  2
Affiliations
Review

Mechanisms of sensorineural cell damage, death and survival in the cochlea

Ann C Y Wong et al. Front Aging Neurosci. .

Abstract

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.

Keywords: age-related hearing loss (ARHL); c-Jun terminal kinase (JNK); cell survival signaling; hair cells (HCs); inflammation; presbycusis; reactive oxygen species (ROS); spiral ganglion neurons (SGN).

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Figures

Figure 1
Figure 1
Illustration highlighting cochlear tissues that are prone to irreversible damage and cell death in SNHL in red. Damage to any of these tissues reduces hearing.
Figure 2
Figure 2
Summary diagram of the survival and damaging factors in the cochlea that require balancing to prevent or delay SNHL.
Figure 3
Figure 3
Cumulative/synergistic damage hypothesis of age-related hearing loss (ARHL). Causes of SNHL that accumulate over a lifetime combine with endogenous susceptibility to exacerbate age-related SNHL.
See this image and copyright information in PMC

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