Biglycan Alleviates Age-Related Muscle Atrophy and Hepatocellular Senescence

Area of Science:

• Muscle physiology
• Gerontology
• Metabolic disorders

Background:

• Myokines are muscle-secreted proteins vital for repair and inter-organ communication.
• Aging reduces muscle mass and myokine secretion, increasing sarcopenia and metabolic disease risk.
• Identifying novel myokines like biglycan (BGN) is crucial for understanding aging.

Purpose of the Study:

• To investigate the role of biglycan (BGN) in aging-related muscle and metabolic tissues.
• To determine BGN's effects on muscle atrophy and hepatocellular senescence.

Main Methods:

• Measured BGN levels in aging humans and mice.
• Assessed BGN's impact on muscle atrophy markers and signaling pathways (AKT/mTOR).
• Examined BGN's effects on liver senescence markers (p21, SASP) and cellular functions (lipid accumulation, ROS).

Main Results:

• BGN levels decreased in aging muscle and plasma but were restored by exercise in mice.
• BGN counteracted muscle atrophy gene expression and mitigated muscle mass loss via AKT/mTOR.
• BGN reduced liver senescence markers, lipid accumulation, and ROS generation.

Conclusions:

• Biglycan (BGN) exhibits protective effects against age-related muscle atrophy.
• BGN also mitigates hepatocellular senescence, suggesting a role in combating age-related metabolic diseases.
• BGN represents a potential therapeutic target for age-related conditions.