Abstract
Presbycusis (age-related hearing loss) is the most universal sensory degenerative disease in elderly people caused by the degeneration of cochlear cells. Non-coding microRNAs (miRNAs) play a fundamental role in gene regulation in almost every multicellular organism, and control the aging processes. It has been identified that various miRNAs are up- or down-regulated during mammalian aging processes in tissue-specific manners. Most miRNAs bind to specific sites on their target messenger-RNAs (mRNAs) and decrease their expression. Germline mutation may lead to dysregulation of potential miRNAs expression, causing progressive hair cell degeneration and age-related hearing loss. Therapeutic innovations could emerge from a better understanding of diverse function of miRNAs in presbycusis. This review summarizes the relationship between miRNAs and presbycusis, and presents novel miRNAs-targeted strategies against presbycusis.
Highlights
Presbycusis is the most universal sensory degenerative disease in elderly people caused by the degeneration of cochlear cells
The results suggest that autophagy is essential for the mir-34 mutants induced lifespan extension and miR-34 may regulate the genes which are associated with the activity of autophagy and control the C. elegans lifespan
These results suggest that reactive oxygen species (ROS) increases in the course of senescence of cochlea with aging, and multiple cell death pathways related to oxidative stress in aging mice are activated in the hair cells of the auditory organ [55]
Summary
Seidman has showed that before cell dysfunction with cell senescence, activity of free oxygen radicals may lead to genetic and cellular alterations [2]. The signs of oxidative stress distinctly increased in the cochlea of male CBA/J mice with aging and increased levels of p38 MAPK and JNK phosphorylation are observed in the cochleae of aging CBA/J mice [54]. These results suggest that reactive oxygen species (ROS) increases in the course of senescence of cochlea with aging, and multiple cell death pathways related to oxidative stress in aging mice are activated in the hair cells of the auditory organ [55]. The study suggests that the variational expression of miRNA induced by ROS may cause the degeneration of Corti be involved in presbycusis [57]
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