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Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles
Published on: November 1, 2012
Calpains in muscle wasting
Marc Bartoli1, Isabelle Richard
1Généthon, Centre National de la Recherche Scientifique UMR 8115, 1 bis rue de l'Internationale, 91000 Evry, France.
Abstract:
Calpains are intracellular nonlysosomal Ca(2+)-regulated cysteine proteases. They mediate regulatory cleavages of specific substrates in a large number of processes during the differentiation, life and death of the cell. The purpose of this review is to synthesize our current understanding of the participation of calpains in muscle atrophy. Muscle tissue expresses mainly three different calpains: the ubiquitous calpains and calpain 3. The participation of the ubiquitous calpains in the initial degradation of myofibrillar proteins occurring in muscle atrophy as well as in the necrosis process accompanying muscular dystrophies has been well characterized. Inactivating mutations in the calpain 3 gene are responsible for limb-girdle muscular dystrophy type 2A and calpain 3 has been found to be downregulated in different atrophic situations, suggesting that it has to be absent for the atrophy to occur. The fact that similar regulations of calpain activities occur during exercise as well as in atrophy led us to propose that the calpains control cytoskeletal modifications needed for muscle plasticity.
Insights
Calpains, calcium-regulated proteases, are involved in muscle atrophy. Ubiquitous calpains initiate myofibrillar protein degradation, while calpain 3 absence is linked to muscle wasting and dystrophy.
Area of Science:
- Biochemistry
- Cell Biology
- Muscle Physiology
Background:
- Calpains are Ca(2+)-regulated cysteine proteases crucial for cellular processes.
- They play roles in cell differentiation, life, and death through substrate cleavage.
Purpose of the Study:
- To review the role of calpains in muscle atrophy.
- To synthesize current understanding of calpain involvement in muscle wasting.
Main Methods:
- Literature review of calpain function in muscle.
- Analysis of calpain expression and activity in atrophic conditions.
- Examination of genetic mutations affecting calpain function.
Main Results:
- Ubiquitous calpains contribute to myofibrillar protein degradation in muscle atrophy and muscular dystrophies.
- Calpain 3 gene mutations cause limb-girdle muscular dystrophy type 2A.
- Calpain 3 is downregulated in atrophic situations, suggesting its absence is necessary for atrophy.
Conclusions:
- Calpains are key regulators in muscle atrophy.
- Calpain 3 plays a critical, potentially protective, role in muscle homeostasis.
- Calpain activity regulation during exercise and atrophy suggests a role in muscle plasticity and cytoskeletal adaptation.
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