Study Reveals How to Prevent Hearing Loss through Use of an Enzyme

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In a latest study, researchers from St. Jude Children’s Research Hospital have found out that prohibiting an enzyme known as cyclin-dependent kinase 2 (CDK2) assists in protecting rats and mice from drug or noise induced hearing loss. It also makes a suggestion that CDK2 inhibitors averts the damage and death of inner ear cells, which also possesses the potential to assist in saving the hearing of millions of people across the globe.

Multiple Compounds Protect Cochlear Cells From Cisplatin

In accordance with the World Health Organization, around 360 million people across the globe, comprising 32 million of children, suffer from hearing loss which is caused by various congenital defects or many other factors. These aforesaid factors comprise exposure to excessive noise, use of certain medicines, or infectious disease. However, there are currently no drugs that are approved by food and drug administration or FDA as it popularly known as so as to treat or avert loss of hearing.

This team of researchers that is led by Dr. Jian Zuo has examined more than 4,000 drugs for their capability to safeguard cochlear cells from cisplatin, chemotherapy agent. Cisplatin is utilized for the purpose of treatment of a variety of cancers but results in irreversible hearing loss in around 70% of the patients worldwide.

Zuo and his colleagues have figured out multiple compounds that safeguarded cochlear cells from cisplatin, many of which have already been approved for the treatment of various other conditions. Three out of the ten most efficacious compounds were inhibitors of an enzyme which is known as CDK2. One of these CDK2 inhibitors, kenpaullone, has been more successful than the other four compounds which are presently in clinical trials for the treatment of hearing loss.

In case of hearing loss that is cisplatin-induced, kenpaullone seems to defend hair cells through prevention of CDK2 from triggering the production of various toxic reactive oxygen species from the cells’ called mitochondria.

The said research has been published on the March issue of Journal of Experimental Medicine.

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