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Targeting dysregulation of redox homeostasis in noise-induced hearing loss: Oxidative stress and ROS signaling.

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Affiliations

  • 1. Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy; Institute of Otolaryngology, Università Cattolica del Sacro Cuore, Rome, Italy; CNR Institute of Cell Biology and Neurobiology, Monterotondo, Italy.
      Authors
    • Fetoni AR 1
    (1 author)
  • 2. Institute of Otolaryngology, Università Cattolica del Sacro Cuore, Rome, Italy; CNR Institute of Cell Biology and Neurobiology, Monterotondo, Italy.
      Authors
    • Paciello F 2
    (1 author)
  • 3. Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy; Institute of Otolaryngology, Università Cattolica del Sacro Cuore, Rome, Italy.
      Authors
    • Rolesi R 3
    • Paludetti G 3
    (2 authors)
  • 4. Institute of Human Physiology, Università Cattolica del Sacro Cuore, Rome, Italy.
      Authors
    • Troiani D 4
    (1 author)

ORCIDs linked to this article

Free Radical Biology & Medicine, 22 Feb 2019, 135:46-59
https://doi.org/10.1016/j.freeradbiomed.2019.02.022 PMID: 30802489 

Review

Abstract 

Hearing loss caused by exposure to recreational and occupational noise remains a worldwide disabling condition and dysregulation of redox homeostasis is the hallmark of cochlear damage induced by noise exposure. In this review we discuss the dual function of ROS to both promote cell damage (oxidative stress) and cell adaptive responses (ROS signaling) in the cochlea undergoing a stressful condition such as noise exposure. We focus on animal models of noise-induced hearing loss (NIHL) and on the function of exogenous antioxidants to maintaining a physiological role of ROS signaling by distinguishing the effect of exogenous "direct" antioxidants (i.e. CoQ10, NAC), that react with ROS to decrease oxidative stress, from the exogenous "indirect" antioxidants (i.e. nutraceutics and phenolic compounds) that can activate cellular redox enzymes through the Keap1-Nrf2-ARE pathway. The anti-inflammatory properties of Nrf2 signaling are discussed in relation to the ROS/inflammation interplay in noise exposure. Unveiling the mechanisms of ROS regulating redox-associated signaling pathways is essential in providing relevant targets for innovative and effective therapeutic strategies against NIHL.

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Read article at publisher's site: https://doi.org/10.1016/j.freeradbiomed.2019.02.022

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Funding 

Funders who supported this work.

BRiC INAIL 2016- DiMEILA17, Italy

    National Grant, Italy

      Università Cattolica del Sacro Cuore (UCSC) Rome, Italy (1)