Ewha Researchers Reveals a Systemic Metabolic Mechanism Linking Liver Disease and Osteoarthritis
Professor Yi-Jun Kim
College of Medicine
Identifies a "liver–cartilage selenium axis" through which impaired liver function accelerates cartilage degeneration
Published in Cell Metabolism (IF 37.0), a top-tier international journal in endocrinology and metabolism
A new systemic metabolic mechanism that explains why liver disease and osteoarthritis so often occur together has been identified.
A research team led by Professor Yi-Jun Kim (College of Medicine, Ewha Womans University), working with Professor Jin-Hong Kim's team at the School of Biological Sciences, Seoul National University, has uncovered a previously unrecognized "liver–cartilage selenium axis." When liver function declines, delivery of selenium, an essential trace element, to joint cartilage is restricted, which in turn promotes chondrocyte senescence and the progression of osteoarthritis.
The study, titled "A liver-cartilage selenium axis underlies metabolic comorbidity in osteoarthritis," was published in the October 2026 issue of Cell Metabolism (IF 37.0), a leading international journal in endocrinology and metabolic biology.
Osteoarthritis is a degenerative joint disease in which the breakdown of articular cartilage causes severe pain and loss of mobility. It has long been regarded as a localized disorder driven mainly by aging and mechanical wear. Growing evidence that osteoarthritis frequently coexists with systemic metabolic diseases such as obesity and diabetes, however, has raised the possibility that metabolic dysfunction in other organs affects joint health as well.
The team focused on the relationship between liver disease and osteoarthritis. Analyses of large-scale population data from Korea and the United States (NHANES, KNHANES, and a nationwide Korean National Health Insurance Service cohort) showed that osteoarthritis is significantly more common in people with liver disease, across etiologies ranging from fatty liver and viral hepatitis to cirrhosis. The team then traced how liver dysfunction leads to cartilage degeneration and identified the liver–cartilage selenium axis as the central mechanism.
Selenium is an essential component of the antioxidant selenoproteins that protect cells from reactive oxygen species. It is distributed throughout the body mainly through selenoprotein P (SELENOP), a carrier protein produced and secreted by the liver. Using mouse models of acute, chronic, and metabolic (MASH) liver injury, the researchers found that liver disease suppresses SELENOP production in hepatocytes at both the transcriptional and translational levels, reducing the amount of selenium carried through the bloodstream to cartilage.
Selenium-deprived chondrocytes lost their antioxidant capacity, accumulated reactive oxygen species, and underwent accelerated cellular senescence, which weakened cartilage maintenance and sped up the progression of osteoarthritis. Consistently, circulating SELENOP was lower in patients with osteoarthritis than in healthy controls, and lowest in patients showing biochemical signs of hepatic stress.
To test whether this shortfall in liver-to-cartilage selenium delivery actually drives osteoarthritis, the team supplemented selenium in several animal models of liver dysfunction. Even while liver function remained impaired, selenium supplementation restored antioxidant selenoproteins in chondrocytes, reduced cellular senescence, and alleviated cartilage damage, joint pain, and the progression of osteoarthritis. Population data pointed in the same direction: among people with liver disease, a daily selenium intake below 90 μg was associated with a 62.1% higher prevalence of osteoarthritis, whereas no such association was seen in people with healthy livers.
Taken together, the findings show that when liver disease disrupts the normal SELENOP-mediated selenium supply, direct dietary selenium supplementation can bypass the damaged liver–cartilage link and suppress the development of osteoarthritis.
Figure caption: Schematic of selenium metabolism between the liver and the joint
"This study shows that osteoarthritis can be triggered not only by problems within the joint itself, but also by the systemic effects of metabolic dysfunction in other organs," said Professor Yi-Jun Kim. "It is a first step toward building selenium-based prevention and treatment strategies tailored to osteoarthritis patients with accompanying liver disease."
Publication and funding
- Paper: Sangmin Yong, Hyewon Jo, et al. "A liver-cartilage selenium axis underlies metabolic comorbidity in osteoarthritis." Cell Metabolism 38 (October 2026).
https://doi.org/10.1016/j.cmet.2026.08.023- Corresponding authors: Professor Yi-Jun Kim (Ewha Womans University) and Professor Jin-Hong Kim (Seoul National University); first author: Sangmin Yong (Seoul National University)
- Funding: The study was supported by the Mid-career Researcher Program and the Bio & Medical Technology Development Program (Next-Generation Bio) of the National Research Foundation of Korea, funded by the Ministry of Science and ICT; the Global Physician-Scientist Training Program of the Korea Health Industry Development Institute, funded by the Ministry of Health and Welfare; the Korea Drug Development Fund; and the Suh Kyungbae Foundation.
Photo caption: (Left) The Ewha Womans University team — from left, Minju Kim (medical student), Hyewon Jo (researcher), and Professor Yi-Jun Kim. (Right) The Seoul National University team — from left, Sangmin Yong (first author) and Professor Jin-Hong Kim (School of Biological Sciences).