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MuRF1/TRIM63, Master Regulator of Muscle Mass
Dulce Peris-Moreno1, Daniel Taillandier1, Cécile Polge1
1INRA, UNH, Unité de Nutrition Humaine, Université Clermont Auvergne, F-63000 Clermont-Ferrand, France.
International Journal of Molecular Sciences
|September 16, 2020
Summary
The E3 ligase MuRF1 (Muscle RING Finger 1) is crucial in skeletal muscle atrophy but also protects the heart. Understanding its dual role is key for developing treatments for muscle wasting diseases.
Area of Science:
- Biochemistry
- Molecular Biology
- Physiology
Background:
- MuRF1 (Muscle RING Finger 1) is an E3 ubiquitin ligase implicated in skeletal muscle atrophy.
- Muscle wasting is linked to poor prognosis in diseases like cancer, sepsis, and diabetes.
- MuRF1 exhibits dual roles, detrimental in skeletal muscle but cardioprotective in the heart.
Purpose of the Study:
- To review 20 years of research on MuRF1's structure, regulation, function, and inhibitors.
- To highlight MuRF1's opposing roles in skeletal and cardiac muscle.
- To inform the design of future drugs targeting MuRF1 for muscle wasting conditions.
Main Methods:
- Literature review of studies on MuRF1 in skeletal and cardiac muscle.
- Analysis of data on MuRF1 structure, regulation, localization, and function.
- Examination of reported MuRF1 inhibitors.
Main Results:
- MuRF1 is a key mediator of skeletal muscle atrophy in catabolic states.
- MuRF1 demonstrates cardioprotective functions, contrasting its role in skeletal muscle.
- The review synthesizes current knowledge on MuRF1's complex biology.
Conclusions:
- MuRF1's dual function necessitates careful consideration for therapeutic strategies.
- Targeting MuRF1 offers potential for treating muscle wasting diseases.
- Further research into MuRF1 characteristics is vital for drug development.
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