Antarctic Fish Reveals 'Muscle Regeneration Switch'... Paving the Way for New Sarcopenia Treatments [Reading Science]

KOPRI Identifies Muscle Regeneration-Inhibiting Protein 'Dnajb5' for the First Time Worldwide
Mouse Experiments Show 26% Increase in Muscle Regeneration and 14% Gain in Strength
New Treatment Approach Offers Hope for Reduced Side Effects

A new therapeutic target for treating sarcopenia, the age-related loss of muscle mass, and cachexia, the severe muscle wasting seen in cancer patients, has been discovered in an Antarctic fish. For the first time in the world, researchers have identified the mechanism of action of a protein that suppresses muscle regeneration, presenting a new therapeutic strategy that may reduce the side effects of existing treatments.

On July 21, the Korea Polar Research Institute announced that Dr. Jin-Hyung Kim’s research team, together with Professor Mi-Seop Yoon’s team at Gachon University, discovered "Dnajb5," a member of the heat shock protein (HSP) family that regulates muscle regeneration and growth in the Antarctic Black Rockfish (Notothenia coriiceps), and elucidated its mechanism of action.

Antarctic Black Rockfish. Photo provided by research team

Sarcopenia is one of the most rapidly increasing age-related diseases as the population ages. According to the 2024 Korea National Health and Nutrition Examination Survey by the Korea Disease Control and Prevention Agency, 1 in 10 Koreans aged 65 or older is affected by sarcopenia. Cachexia, which occurs in cancer patients, is also considered a major factor that significantly deteriorates treatment outcomes and quality of life.

Although candidate substances for promoting muscle growth have been developed, the side effects—such as systemic metabolic disorders, insulin resistance, and increased cancer risk—have remained significant limitations.

'Double Brake' Releases Muscle Regeneration

The research team analyzed the muscles of the Antarctic Black Rockfish, which survives in highly oxidative and extremely cold environments, and found that Dnajb5 is a key protein regulating muscle regeneration.

Under normal conditions, Dnajb5 acts as a "double brake," simultaneously suppressing both protein synthesis and energy production pathways within the muscle. However, when the muscle is damaged or under stress, its binding strength weakens, releasing both brakes at once and activating muscle regeneration and growth functions.

The research team also confirmed this effect through experiments with mice. When muscle damage was induced and the expression of Dnajb5 was inhibited, the cross-sectional area of regenerated muscle fibers increased by about 26% compared to the control group. Muscle strength improved by 14%, and endurance was maintained for 31% longer, indicating an overall improvement in physical performance.

Dnajb5 Protein Mechanism of Action. Provided by the Research Team

The research team explained that activating both protein synthesis and energy metabolism pathways simultaneously led to improved physical strength and increased intracellular metabolic efficiency of the muscle.

Jin-Hyung Kim, principal researcher at the Korea Polar Research Institute, stated, "Dnajb5 is a protein found abundantly and selectively in muscle tissue. Targeting only this protein could minimize the systemic side effects of conventional treatments and allow for a safer induction of muscle regeneration."

The results of this research were published in the July issue of the international journal Journal of Cachexia, Sarcopenia and Muscle, which focuses on muscle biology and geriatric medicine.

Hyung-Chul Shin, director of the Korea Polar Research Institute, said, "This study shows that the survival strategies of polar organisms, which have adapted to extreme environments, can hold the key to treating intractable human diseases. It once again demonstrates the medical potential of polar biological resources."

This content was produced with the assistance of AI translation services.