Cochlear implantation trauma and noise-induced hearing loss: Apoptosis and therapeutic strategies.
Cochlear implantation trauma and noise-induced hearing loss both involve a physical disruption of the organ of Corti and may involve several mechanisms of cell death at the molecular level, i.e., necrosis, necrosis-like programmed cell death (PCD; type 2 PCD), and apoptosis (type 1 PCD). This article reviews several promising therapeutic strategies that are currently being developed. One of these promising new strategies involves the use of a highly effective peptide inhibitor of the c-Jun N-terminal kinase cell death signal cascade (i.e., D-JNKI-1) to prevent apoptosis of injured auditory hair cells. Our recent studies showed prevention of cochlear implantation-induced hearing loss by infusing this peptide into the cochlea of guinea pigs. Another otoprotective therapy under investigation is the application of mild hypothermia to protect the cochlea from the development of a hearing loss that follows exposure to a physical trauma, e.g., electrode array insertional trauma. These forward-looking strategies have the potential of improving hearing outcomes after cochlear implantation and providing novel means of otoprotection from noise-induced trauma.
University of Miami Ear Institute, Department of Otolaryngology, University of Miami, Miller School of Medicine, Miami, Florida 33136, USA.
Adrien A
AA
Eshraghi
Thomas R
TR
Van de Water
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D019929:Cochlear Implantation / Q000009:adverse effects*; D004594:Electrophysiology; D006317:Hearing Loss, Noise-Induced / Q000628:therapy*; D006801:Humans; D007035:Hypothermia; D048031:JNK Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors; D009925:Organ of Corti / Q000293:injuries*; D010455:Peptides / Q000627:therapeutic use*
D010455:Peptides; D048031:JNK Mitogen-Activated Protein Kinases; C478085:D-JNKI-1