Integrative functional transcriptomic analyses implicate shared molecular circuits in sensorineural hearing loss

Aging, noise exposure, and ototoxic drugs represent the three main causes of SNHL, leading to substantial similarities in pathophysiological characteristics of cochlear degeneration. Although the common molecular mechanisms are widely assumed to underlie these similarities, its validity lacks systematic examination. To address this question, we generated three SNHL mouse models from aging, noise exposure, and cisplatin ototoxicity and constructed gene coexpression networks for the cochlear transcriptome data across different hearing-damaged stages. Overall design: The cochleae were harvested from controls (2-month-old mice), aging-induced SNHL (8-month-old and 12-month-old mice), noise-induced SNHL (2-month-old female mice after being exposed to noise for one hour and 2-month-old mice after being exposed to noise for 24 hours), and cisplatin-induced SNHL (2-month-old mice after being injected with cisplatin for one day and 2-month-old mice after being injected with cisplatin for three days). An individual's bilateral cochleae were collected as a biological replicate. To ensure the reliability and repeatability of our data, at least three replicates were required.