Discovery of c-Kit protein’s protective role could help explain why sweetness lingers when other tastes fade
SEOUL, South Korea, Oct. 6, 2025 /PRNewswire/ — 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.
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 In organoid cultures, these cells continued to grow even when survival factors were withdrawn.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.”
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.
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.
Reference
Title of original paper: c-Kit signaling confers damage-resistance to sweet taste cells upon nerve injury
Journal: International Journal of Oral Science
DOI: 10.1038/s41368-025-00387-3
Website: https://medicine.korea.ac.kr/en/index.do
Media Contact:
Soo-Jin Jeon
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SOURCE Korea University College of Medicine
