AI Article Synopsis
- - Age-related hearing loss (ARHL), or presbyacusis, results mainly from degeneration in sensory cells of the auditory system and is linked to increased reactive oxygen species (ROS) and inflammatory responses in the aging cochlea.
- - Research using various methods found elevated levels of activated proteins and inflammatory markers (like Caspase-1 and interleukins) in the inner ears of older mice compared to younger ones.
- - The study suggests that inflammation from inflammasome activation in the cochlea could play a significant role in the development of ARHL, indicating a potential target for addressing age-related hearing loss.
Article Abstract
Age-related hearing loss (ARHL) or presbyacusis is a progressive loss of hearing sensitivity that is predominately associated with sensory or transduction neuro-cell degeneration in the peripheral and central auditory systems. Increased production of reactive oxygen species (ROS) and inflammatory response were frequently found in aging cochleae. In addition, inflammasomes are likely responsible for the accumulation of ROS in immune cells, although whether they are in fact involved in the development of ARHL is unknown. In this study, Q-PCR, WB and ELASA demonstrated significantly increased levels of activated Caspase-1, interleukin-1β and interleukin-18 and even NLRP3 in the inner ears of aging mice compared to younger one. In addition, NLRP3, as a sensor protein of ROS, may contribute to inflammasome assembly and subsequent inflammation in the cochleae. In conclusion, inflammation triggered by the activation of inflammasomes in the cochleae of aging mice appears to be playing an important role in the pathological process of ARHL and may be a potential cause of presbyacusis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5752911 | PMC |
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