Found Treatment for Degenerative Arthritis: "Selenium Protein Deficiency is the Cause"

Seoul National University Research Team Publishes Paper in Nature Communications

[Asia Economy Reporter Kim Bong-su] The cause of cartilage cell aging, which has been identified as a cause of osteoarthritis, has been revealed.

Seoul National University announced on the 17th that a research team led by Professors Kim Jin-hong and Lee Byung-jae from the Department of Life Sciences published a paper in the international journal Nature Communications on the 9th, elucidating the joint-protective effects of selenium metabolism and providing clues for treatment strategies for osteoarthritis based on this.

Osteoarthritis is a disease in which cartilage wears away due to frequent use of joints, and its prevalence increases with age. As cartilage degenerates, patients experience pain and limited movement whenever they move their joints, significantly reducing their quality of life. Globally, 29.5% of the population aged 60 and over suffer from osteoarthritis, and the number of patients is expected to continue increasing due to population aging.

There is currently no fundamental cure for osteoarthritis. At present, the best method is joint replacement surgery, which replaces the degenerated cartilage with an artificial joint, but this is not a fundamental solution. Therefore, it is necessary to discover new treatment strategies through research on the pathogenesis of osteoarthritis.

Recently, a domestic research team applied the antioxidant concept of selenium metabolism to cartilage tissue, achieving research results that prevent cartilage cell aging and alleviate osteoarthritis. Osteoarthritis is known to be caused by cellular aging resulting from disrupted redox homeostasis within cartilage cells. The research team identified the selenium metabolic enzyme SEPHS1 as a regulator that maintains redox homeostasis in cartilage cells. In osteoarthritic cartilage cells, the expression of SEPHS1 decreased, leading to a significant reduction in the expression of selenium proteins with antioxidant functions. As a result, DNA damage and cellular aging accompanied the progression of osteoarthritis. This pathological phenomenon was confirmed not only at the molecular biological level but also at the histological and behavioral levels using an osteoarthritis animal model after antioxidant administration. This study is the first to propose a path for osteoarthritis treatment using SEPHS1, a regulator that can prevent cartilage cell aging.

This study is the first to clarify the causal relationship between selenium metabolism, which has been suggested to have antioxidant functions, and osteoarthritis. It also revealed that the decrease in SEPHS1 is a cause of aging in cartilage cells subjected to stress such as aging or physical impact. The study suggested that both dietary selenium and selenium metabolism in the body are important for preserving joint health. A treatment strategy for osteoarthritis through selenium intake is expected to satisfy the needs of various patient groups in the future, as it presents a lower barrier to entry for patients compared to drugs or surgery.

The research team stated, "It is significant that we provided biological evidence that abnormal selenium metabolism within cells causes disease," and added, "We will develop methods for selenium intake that can effectively protect joints."

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