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Published on: October 15, 2019
Forkhead Box O Signaling Pathway in Skeletal Muscle Atrophy
Kun Chen1, Peng Gao1, Zongchao Li1
1Department of Orthopaedics, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.
Abstract:
Skeletal muscle atrophy is the consequence of protein degradation exceeding protein synthesis because of disease, aging, and physical inactivity. Patients with skeletal muscle atrophy have decreased muscle mass and fiber cross-sectional area, and experience reduced survival quality and motor function. The forkhead box O (FOXO) signaling pathway plays an important role in the pathogenesis of skeletal muscle atrophy by regulating E3 ubiquitin ligases and some autophagy factors. However, the mechanism of FOXO signaling pathway leading to skeletal muscle atrophy is still unclear. The development of treatment strategies for skeletal muscle atrophy has been a thorny clinical problem. FOXO-targeted therapy to treat skeletal muscle atrophy is a promising approach, and an increasing number of relevant studies have been reported. This article reviews the mechanism and therapeutic targets of the FOXO signaling pathway mediating skeletal muscle atrophy, and provides ideas for the clinical treatment of this condition.
Insights
Skeletal muscle atrophy, driven by protein breakdown, involves the FOXO signaling pathway. Targeting FOXO offers a promising therapeutic strategy for this condition.
Area of Science:
- Biochemistry
- Cell Biology
- Physiology
Background:
- Skeletal muscle atrophy results from imbalanced protein synthesis and degradation.
- It leads to reduced muscle mass, impaired motor function, and decreased quality of life.
- The forkhead box O (FOXO) signaling pathway is implicated in muscle atrophy pathogenesis.
Purpose of the Study:
- To review the mechanisms by which the FOXO signaling pathway mediates skeletal muscle atrophy.
- To identify therapeutic targets within the FOXO pathway for treating muscle atrophy.
- To provide insights for clinical treatment strategies.
Main Methods:
- Literature review of studies on FOXO signaling and skeletal muscle atrophy.
- Analysis of the role of FOXO in regulating protein degradation and autophagy.
- Examination of current and potential therapeutic interventions targeting FOXO.
Main Results:
- FOXO signaling regulates key E3 ubiquitin ligases and autophagy factors involved in muscle protein breakdown.
- The precise molecular mechanisms linking FOXO to atrophy are still under investigation.
- FOXO-targeted therapies represent a promising avenue for treating skeletal muscle atrophy.
Conclusions:
- The FOXO signaling pathway is a critical regulator in skeletal muscle atrophy.
- Understanding FOXO's role is essential for developing effective treatments.
- Targeting FOXO presents a viable strategy for clinical intervention in muscle wasting conditions.
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