July 28, 2006Human Molecular GeneticsOpen Access

Skeletal muscle repair in a mouse model of nemaline myopathy

Q: What is the clinical evidence from this study?

Study design: Other. Population: Nemaline myopathy. Intervention: Met9Arg mutation of alpha-tropomyosin slow (Tpm3) vs. Non-affected mice. Primary outcome: Gene expression patterns and markers of muscle repair.

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Key result

A mouse model of nemaline myopathy carrying the human Met9Arg mutation of Tpm3 demonstrated elevated markers of satellite cells and immature fibers, indicating a novel repair process.

Authors

DSDespina SanoudouNational and Kapodistrian University of Athens MCMark CorbettSA Health MHMei HanHebei Medical University

Discussion

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Implication

Does not support clinical translation; leaves open a novel satellite cell repair mechanism in nemaline myopathy for human validation.

PICO

Population

Nemaline myopathy

Intervention / Comparator

Met9Arg mutation of alpha-tropomyosin slow (Tpm3) vs Non-affected mice

Primary Outcome

Gene expression patterns and markers of muscle repair

Cite This Study

Sanoudou et al. (2006) studied Nemaline myopathy. Met9Arg mutation of alpha-tropomyosin slow (Tpm3) vs. Non-affected mice was evaluated on Gene expression patterns and markers of muscle repair. A mouse model of nemaline myopathy carrying the human Met9Arg mutation of Tpm3 demonstrated elevated markers of satellite cells and immature fibers, indicating a novel repair process.

synapsesocial.com/papers/6a0908d8bee8d5ab8a92dbef https://doi.org/10.1093/hmg/ddl186

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Skeletal muscle repair in a mouse model of nemaline myopathy

Discussion

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Implication

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Cite This Study

Skeletal muscle repair in a mouse model of nemaline myopathy

Discussion

Member takes

Implication

PICO

Cite This Study

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