LCN2 promotes HEI-OC1 cells senescence via activating NF-κB signal pathway in presbycusis.
Many older adults experience a gradual decline in hearing, a condition known as age-related hearing loss, or presbycusis. While common, the exact molecular reasons behind why our hearing deteriorates with age have remained unclear. Recent research has shed light on this mystery by identifying a key protein involved in this process.
Scientists discovered that a protein called LCN2 plays a significant role in the aging of cells within the inner ear. When levels of this protein are elevated, it appears to accelerate a process known as cellular senescence. Senescence is when cells stop dividing and enter a state of irreversible growth arrest, often leading to their malfunction or accumulation, contributing to aging and age-related diseases. Conversely, reducing the amount of LCN2 was shown to delay this cellular aging.
How does LCN2 achieve this? The study revealed that LCN2 acts by activating a crucial cellular communication system called the NF-κB signaling pathway. This pathway is a central regulator of many cellular processes, including inflammation, stress responses, and cell survival. Its activation by LCN2 seems to be a critical step in promoting the senescence of auditory cells.
These findings offer valuable new insights into the underlying mechanisms of age-related hearing loss. By identifying LCN2 as a key factor and detailing its interaction with the NF-κB pathway, this research opens up new possibilities for developing targeted treatments. Future therapies might focus on modulating LCN2 levels or inhibiting the NF-κB pathway to potentially prevent or slow the progression of age-related hearing loss.