Abstract
Hearing loss is often caused by death of sensory hair cells (HCs) in the inner ear. HCs are vulnerable to some ototoxic drugs, such as aminoglycosides(AGs) and the cisplatin.The most predominant form of drug-induced cell death is apoptosis. Many efforts have been made to protect HCs from cell death after ototoxic drug exposure. These mechanisms and potential targets of HCs protection will be discussed in this review.And we also propose further investigation in the field of HCs necrosis and regeneration, as well as future clinical utilization.
Highlights
Hearing loss is the most common sensory impairment in humans
Hearing loss is often caused by death of sensory hair cells (HCs) in the inner ear, which function in transducing the sound waves into electric signals [2,3,4,5,6]
Some researchers suggest AGs and cisplatin can enter the HCs through mechanoelectrical transducer (MET) channel [25, 29, 30] or Copper Transporter 1 (CTR1) [31], respectively, which are located at the top of hair cell stereocilia
Summary
Hearing loss is the most common sensory impairment in humans. It is estimated that there were 466 million people living with hearing loss in 2018 [1]. The ototoxicity limits the clinical application of these two kinds of drugs Both AGs and cisplatin can induce apoptotic cell death in HCs, especially the outer HCs of the basal turn [9, 19,20,21,22,23]. In order to protect HCs from ototoxic insult, a better understanding of the mechanisms of aminoglycosideand cisplatin-induced hair cell death is required. Current studies of these apoptotic cell death mechanisms and potential targets of HC protection are discussed in this review
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