Cell destruction is essential for improving hearing

A recent study published in the journal Cell Death & Disease found that autophagy—a form of cell destruction—is essential for hearing in mouse models. Autophagy is a normal process by which the body deals with damaged or unnecessary cell components, but this study gives us further insight into potential treatment of hearing loss.

Hearing loss is the most common sensory disorder in humans. In fact, 360 million people worldwide are currently experiencing disabling hearing loss. The most common cause of hearing loss is damage to auditory hair cells. This can be caused by a number of different factors, such as aging or exposure to intense noise. As auditory hair cells are no longer capable of cell division, they do not regenerate after loss. Because of this, maintaining the function of these auditory hair cells is critical to hearing preservation.

In the study by Chisato Fujimoto and colleagues at the University of Tokyo, mice were generated with a deficiency in the gene Atg5, which is essential for autophagy. The deletion of this gene resulted in autophagy-deficient auditory hair cells, leading to profound hearing loss, as well as progressive degeneration of cells.

Chisato Fujimoto’s team recorded auditory brainstem responses in young mice (at 4 weeks and 8 weeks of age) to demonstrate that deficiencies in the protein Atg5 can lead to significant hearing loss. Conversely, Atg5 in hair cells is crucial in developing normal hearing abilities. It is critical that the function of hair cells is maintained for normal hearing, and this appears to be accomplished via autophagy.

This is not the first study to demonstrate the significance of autophagy in the prevention of auditory damage. Treatment with the autophagy activator rapamycin has shown promise in other studies by alleviating the loss of auditory hair cells in both rats and mice. However, in a context where hearing loss is extremely common in humans, Chisato Fujimoto and his colleagues have shed light on some of the cellular mechanisms that can contribute to hearing loss.

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