Melatonin Regulates Rheumatoid Synovial Fibroblasts-Related Inflammation: Implications for Pathological Skeletal...

Area of Science:

• Immunology
• Molecular Biology
• Muscle Physiology

Background:

• Melatonin regulates circadian rhythms and possesses anti-inflammatory properties.
• Its role in rheumatoid arthritis (RA)-related muscle atrophy is not well-established.

Purpose of the Study:

• To investigate the effects of melatonin on pathological muscle atrophy in rheumatoid arthritis (RA).
• To elucidate the underlying molecular mechanisms of melatonin's action in RA-associated muscle atrophy.

Main Methods:

• Bioinformatic analysis of melatonin's effect on pro-inflammation and myogenesis in RA synovial fibroblasts (RASF) and myoblasts.
• In vitro experiments using conditioned medium from melatonin-treated RASF on myoblasts.
• In vivo study using a collagen-induced arthritis (CIA) mouse model.

Main Results:

• Melatonin regulated the correlation between pro-inflammation and myogenesis in RA cells.
• Melatonin mitigated pro-inflammation and atrophy in myoblasts via NF-κB signaling.
• Melatonin administration improved arthritis symptoms and muscle atrophy in a CIA mouse model.
• Identified miR-30c-1-3p as a novel regulator in this pathway.

Conclusions:

• Melatonin demonstrates a therapeutic effect against RA-induced pathological muscle atrophy.
• Melatonin acts by decreasing inflammation and enhancing myogenesis through NF-κB signaling.
• This study provides evidence for melatonin as a potential therapeutic agent for RA-related muscle wasting.