Focal adhesion kinase and its role in skeletal muscle

J Muscle Res Cell Motil, 2015 · DOI: 10.1007/s10974-015-9415-3 · Published: October 1, 2015

Simple Explanation

Skeletal muscle adapts to physical stresses. Exercise leads to muscle growth, while inactivity causes muscle loss. Focal adhesion kinase (FAK) mediates these changes by translating cytoskeletal signals. FAK is activated by integrins, which transmit stress signals across the cell membrane. This activation triggers pathways that promote cell growth and prevent cell death. FAK regulates costamere formation, muscle growth (hypertrophy), and glucose metabolism. It is crucial for maintaining muscle cell health.

Study Duration

Not specified

Participants

Not specified

Evidence Level

Review

Key Findings

1
Changes in FAK expression and phosphorylation correlate with myoblast differentiation, muscle fiber formation, and muscle size changes due to loading and unloading.
2
FAK is activated by growth factors like insulin and IGF-1 and can regulate myoblast development and muscle fiber formation.
3
FAK may have a role in actin dynamics and most likely functions through activation of RhoA and downstream signaling through FAK and serum response factor (SRF).

Research Summary

This review focuses on the role of focal adhesion kinase (FAK), a prominent and well-studied protein that responds to changes in cellular tension. FAK has multiple roles within skeletal muscle, including regulation of myoblast development and muscle fiber formation. The role of FAK in skeletal muscle provides important insight into how myogenesis and muscle homeostasis is regulated by integrated responses of multiple signaling pathways.

Practical Implications

Therapeutic Potential

Targeting FAK could help protect against muscle atrophy in conditions like SCI, cachexia, and sarcopenia.

Exercise Intervention Strategies

Understanding FAK's role may lead to optimized exercise regimens for muscle health.

Drug Development

Pharmaceutical interventions that modulate FAK activity could be developed to combat muscle wasting.

Study Limitations

1
Limited information regarding the RhoA/FAK/SRF pathway in muscle.
2
Sparse literature on cytokine signaling modulating FAK expression in skeletal muscle.
3
Lack of evidence regarding cSrc’s role in skeletal muscle hypertrophy.

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