MieroRNAs in Noise-Induced Hearing Loss and their Regulation by Oxidative Stress and Inflammation

Noise exposure (NE) has been recognized as one of the causes of sensorineural hearing loss (SNIIL), which can bring about irreversible damage to sensory hair cells in the cochlea, through the launch of oxidative stress pathways and inflammation. Accordingly, determining the molecular mechanism involved in regulating hair cell apoptosis yin NE is essential to prevent hair cell damage. However, the role of micruRNAs (miRNAs) in the degeneration of sensory cells of the cochlea during NE has not been so far uncovered. Thus, the main purpose of this study was to demonstrate the regulatory role of miRNAs in the oxidative stress pathway and inflammation induced by NE. In this respect, articles related to noise-induced hearing loss (NIHL), oxidative stTess, inflammation, and miRNA from various databases of Directory of Open Access Journals (DOAJ), Google Scholar, PubMed; Library, Infonnation Science & Technology Abstracts (LISTA), and Web of Science were searched and retrieved. The findings revealed that several studies had suggested that up-regulation of miR-1229-5p, miR-451a, 185-5p, 186 and down-regulation of miRNA-96/182/183 and miR-30b were involved in oxidative stress and inflammation which could he used as hiomarkers for NIIIL. There was also a close relationship between NIHL and mi RNAs, but further research is required to prove a causal association between miRNA alterations and NE, and also to determine miRNAs as hiomarkers indicating responses to NE.