News Release

Korea University researchers find sweet taste cells resist nerve damage through c-Kit protein

Discovery of c-Kit protein’s protective role could help explain why sweetness lingers when other tastes fade

Peer-Reviewed Publication

Korea University College of Medicine

Sweet Taste Cells Defy Nerve Damage

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Sweet-sensing taste cells, supported by the protein c-Kit, show remarkable resilience when nerves are damaged, unlike other taste cells that quickly degenerate. Blocking c-Kit with the drug imatinib (Gleevec) eliminates these surviving sweet cells, highlighting the protein’s key role in preserving sweetness even after injury.

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Credit: Korea University College of Medicine

Taste is one of our most vital senses, shaping appetite, nutrition, and quality of life. Yet taste buds are fragile, relying heavily on the nerves that connect them to the brain. When those nerves are cut or damaged, taste buds usually deteriorate — but later regenerate as nerves regrow. How this recovery occurs has remained unclear. 

Now, a study led by Dr. Dong-Hoon Kim and Professor Yong Taek Jeong at Korea University College of Medicine, published in the International Journal of Oral Science on September 10, 2025, reveals the key players in this process. The team discovered that sweet-sensing taste cells survive nerve injury thanks to a protein called c-Kit — and that these cells are essential for taste bud regeneration.

Using mouse models and taste bud organoids, the researchers showed that when c-Kit signaling was blocked with the cancer drug imatinib (Gleevec), the surviving sweet cells disappeared. Without these cells, other taste cells failed to regenerate, proving that c-Kit signaling underpins both survival and recovery.

To understand the significance of these findings and what they mean for everyday taste, the researchers spoke about their work in more detail.

Q: What do your findings reveal about taste buds?
Prof. Jeong explained, “Our taste buds are made up of various cells that detect different flavors like sweet, bitter, salty, sour, and umami. It's long been known that these taste buds are closely connected to our taste nerves, as they are where the initial taste signals are formed before being sent to the brain.”

Jeong’s team confirmed what scientists have known for decades — that when the nerves to a taste bud are cut, the bud degenerates and later regenerates as the nerves regrow. But their study advanced this understanding by showing that the extent of degeneration and recovery depends on the type of taste cell involved, with sweet-sensing cells proving far more resilient than other types. This helps explain everyday changes in taste — for example, during a common cold, when some taste qualities fade faster than others because the underlying taste cells adapt differently.

Q: How did you test resilience and what else did you discover about recovery?

We used nerve transection in mice to mimic injury and found that c-Kit–expressing sweet cells consistently survived. In organoid cultures, these cells continued to grow even when survival factors were withdrawn. But when we blocked c-Kit with imatinib, the surviving sweet cells disappeared and regeneration was delayed.

We also discovered that it’s not just sweet cells that matter. Some Type III cells acquired stem-like properties, helping repair the epithelial lining around taste buds. This shows that multiple cell types are involved in recovery — c-Kit+ sweet cells lead regeneration, while Type III cells contribute to repair,” Prof. Jeong said.

Q: What could this mean for the future of taste research?
This is the first discovery that allows us to selectively control specific types of taste cells. While it does not immediately translate into treatment, it provides a foundation for future work on taste resilience and recovery. In the long term, this could guide new approaches to improving nutrition, supporting patients with taste disorders, and even advancing flavor science. By identifying c-Kit as a key factor in sweet cell survival, we now have a building block for more precise control over taste,” Jeong noted.

This study shows that c-Kit–expressing sweet cells are central to taste bud regeneration after nerve injury, with Type III cells also contributing through repair. By identifying c-Kit as a protective factor, the research explains why some taste qualities persist longer than others and lays the groundwork for future efforts to selectively control taste.

 

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Reference
DOI: 10.1038/s41368-025-00387-3

 

About Korea University College of Medicine
Korea University College of Medicine is the medical school of Korea University. It is located in Seoul, South Korea. As one of the oldest medical schools in South Korea, it has been historically regarded as one of the country's top medical schools. The school was founded as Chosun Women's Medical Training Institute in 1928 by Rosetta Sherwood Hall. The institute was subsequently renamed several times and ultimately merged with Korea University to become Korea University College of Medicine. So far, the school has produced over 7,000 graduates, most of whom are working as prominent physicians and public health advocates worldwide.

Website: https://medicine.korea.ac.kr/en/index.do



About the author
Dr. Yong Taek Jeong is an Associate Professor of the Department of Pharmacology at Korea University College of Medicine. His group investigates how our sense of taste is generated, relayed, and processed. His group utilizes advanced research techniques such as organoids, adeno-associated virus, and various neurogenetic tools to study the entire taste system, from taste buds to the brain. Before joining Korea University, he completed the Postdoctoral training in Seok Jun Moon’s lab at Yonsei University College of Dentistry, where he also earned his PhD in 2016.

Dr. Dong-Hoon Kim is a researcher in the Department of Pharmacology at Korea University College of Medicine, Seoul, Republic of Korea, and a member of the BK21 Graduate Program in Biomedical Sciences. His research focuses on molecular and cellular mechanisms underlying sensory biology and regenerative medicine.


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