Scientists at the Del Monte Institute recently published a study in Frontiers in Cellular Neuroscience describing some of the mechanisms behind cochlear hair cell regeneration in mammals. Hearing loss is a common problem affecting millions worldwide, particularly throughout the aging process.

While there are multiple causes of hearing loss, the most common reason is progressive. Primary cells and cochlear hair cells, responsible for interpreting and integrating sound waves, cannot regenerate if they are damaged or lost. People exposed to loud noises repeatedly, such as military personnel, construction workers, and musicians, are at the highest risk for hearing loss.

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The study found that activating the growth gene ERBB2 pathway triggered a series of cellular events that led to cochlear support cells multiplying and activating other neighboring stem cells to become new sensory hair cells.

Single-cell RNA sequencing in mice was used to compare cells with an overactive growth gene with similar cells that lacked such signaling. The results showed that the growth gene ERBB2 promoted stem cell-like development by initiating the expression of multiple proteins, including SPP1, a protein that signals through the CD44 receptor, which is present in cochlear-supporting cells.

The researchers revealed that ERBB2 expression drove the protein expression of SPP1, which is necessary to activate CD44 and grow new hair cells. This discovery has made it clear that, contrary to popular belief, regeneration is not restricted to the early stages of development and that the researchers believe they can use these findings to drive regeneration in adults. The ultimate goal of the study is to determine whether this phenomenon can improve auditory function after damage in mammals.

This study offers new hope for people suffering from hearing loss due to the death of cochlear hair cells. The findings suggest that it may be possible to regenerate these hair cells in adults, and the researchers plan to investigate this phenomenon further from a mechanistic perspective.