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Updated: Jun 20, 2025
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Identification, Isolation, and Characterization of Fibro-Adipogenic Progenitors FAPs and Myogenic Progenitors MPs in Skeletal Muscle in the Rat
Published on: June 9, 2021
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RBP4 promotes denervation-induced muscle atrophy through STRA6-dependent pathway
Kang-Zhen Zhang1, Jia-Wen Li1, Jin-Shui Xu2
1Department of Geriatrics, Zhongda Hospital, School of Medicine, Southeast University, No. 87 Dingjiaqiao, Nanjing, Jiangsu, China.
Journal of Cachexia, Sarcopenia and Muscle
|July 20, 2024
Summary
Retinol binding protein 4 (RBP4) promotes muscle atrophy and fat infiltration via the STRA6/JAK2/STAT3 pathway. Lowering RBP4 levels may offer a therapeutic strategy for muscle wasting disorders.
Area of Science:
- Muscle physiology and cellular biology
- Endocrinology and metabolic research
- Biochemistry of adipokines and signaling pathways
Background:
- Fat infiltration is common in degenerative muscle disorders.
- Retinol binding protein 4 (RBP4) correlates with sarcopenia severity.
- The precise role of RBP4 in muscle atrophy is not fully understood.
Purpose of the Study:
- To elucidate the mechanism by which RBP4 contributes to muscle atrophy.
- To investigate the role of RBP4 in denervation-induced skeletal muscle atrophy.
- To explore potential therapeutic targets for muscle wasting.
Main Methods:
- Utilized a denervation-induced muscle atrophy mouse model.
- Manipulated RBP4 expression via injections and oral gavage of an RBP4 inhibitor.
- Investigated the STRA6/JAK2/STAT3 signaling pathway in C2C12 myotubes and mouse models.
Main Results:
- RBP4 expression increased significantly in denervated muscles, localized to fatty infiltrates.
- RBP4 knockout protected against muscle atrophy; holo-RBP4 exacerbated it.
- The STRA6/JAK2/STAT3 pathway mediates RBP4's effects on muscle atrophy markers.
Conclusions:
- RBP4 promotes fat infiltration and muscle atrophy through a STRA6-dependent, JAK2/STAT3-mediated mechanism.
- Targeting RBP4 presents a potential therapeutic avenue for muscle atrophy.
- RBP4 inhibition ameliorates denervation-induced muscle wasting.
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