n this study, it was discovered that when the peptides located at the N-terminus of potassium channel proteins or peptides with the same or greater levels of amino acid sequence homology with the peptides were administered, the function of those potassium ion channels improved. This study described a methodology for improving the functionality of KCNQ4 potassium ion channel in biological samples and for preventing symptoms of disease affecting potassium channel. More specifically, this method aimed to effectively recover the functionality of potassium channel in addressing problems that lead to non-syndromic, progressive hearing impairment.
n the process of hearing, the voltage-gated potassium channel KCNQ4 plays an important role mainly in the outer hair cells of the cochlea, located within the inner ear. Within the cochlea, maintaining a consistant level of K+ is crucial and KCNQ4 plays essential roles in maintainoing ion homeostasis.. KCNQ4 mutations cause deafness nonsyndromic autosomal dominant 2 (DFNA2), which is characterized by progressive sensorineural hearing loss at all frequencies, Despite numerous studies on the prevention and treatment of hearing loss, the molecular mechanisms behind and the relevant measures that can be taken to treat and prevent the onset of this disease are still unclear. As such, antibiotics and anti-inflammatory medications are the main options available for treating populations faced with the onset of hearing impairment. Taking this into consideration, there is a clear need for the development of effective treatment options that can address the sensorineural basis of hearing loss by returning functionality to damaged ion channel proteins. The technology presented here differed from popular treatment methods for potassium channel irregularities by providing a method that can effectively be implemented to directly remove the source of hearing impairment.