Professor Kyungah Cho's Chonnam National University Research Team Identifies the Role of TLR5 in Liver Function

Published Online in the International Journal 'Aging Cell'
Suggesting the Potential for Treating Metabolic Diseases and Liver Fibrosis

Kyungah Cho, Professor at Chonnam National University.

The research team led by Professor Cho Kyunga from Chonnam National University College of Medicine recently published their findings on the role of TLR5 (Toll-like Receptor 5) in regulating liver function in the international journal ‘Aging Cell’ (Impact Factor 8.0, top 10% Q1 journal in the field of aging) on June 24.

Professor Cho Kyunga's team had previously demonstrated that activation of TLR5 contributes to improved brain metabolic function, suppression of chronic inflammation, lifespan extension, and overall health enhancement.

In this study, the team specifically analyzed the liver metabolic regulatory function of TLR5 and suggested the potential for treating metabolic diseases and liver fibrosis using this mechanism.

TLR5 is an innate immune receptor that recognizes flagellin, a protein of bacterial flagella, and is known to play multifaceted roles in regulating not only immune responses but also metabolism and tissue regeneration.

Using a TLR5-deficient mouse (TLR5 KO) model, the team analyzed age-related changes and confirmed that weight gain, worsening of fatty liver, and metabolic abnormalities were accelerated. Genetic analysis revealed that TLR5 is involved in regulating genes related to fat absorption, breakdown, biosynthesis, storage, circadian rhythm, and cellular aging.

Notably, the team identified a new metabolic regulatory mechanism by demonstrating that TLR5 directly regulates liver metabolic function, rather than metabolic abnormalities arising from the previously known gut-liver axis in the TLR5 KO model. Furthermore, when intestinal inflammation and liver fibrosis were induced separately in the TLR5 KO model, only liver fibrosis worsened, confirming that TLR5 is directly involved in liver metabolic regulation.

Additionally, the team demonstrated the improvement of metabolic function and therapeutic effects on liver fibrosis by using an improved flagellin-based therapeutic agent in animal models of metabolic disease and liver fibrosis. This study was conducted in collaboration with MediSpan. The technology used in the research is based on substances that have been transferred to MediSpan.

A MediSpan representative stated, “This research is an important achievement that once again proves the potential of MediSpan’s core technology, and we plan to further accelerate the development of therapeutics for metabolic diseases utilizing TLR5.”

Professor Cho said, “TLR5 plays an essential role in maintaining liver function and metabolic homeostasis and can be an important target for treating metabolic diseases. If we deeply understand and enhance immune function, it will be possible to achieve healthy aging and longevity.”