Medicine:Myostatin-related muscle hypertrophy

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Myostatin-related muscle hypertrophy is a rare genetic condition characterized by reduced body fat and increased skeletal muscle size.[1] Affected individuals have up to twice the usual amount of muscle mass in their bodies, but increases in muscle strength are not usually congruent.[2] Myostatin-related muscle hypertrophy is not known to cause medical problems, and affected individuals are intellectually normal. The prevalence of this condition is unknown.

Mutations in the MSTN gene cause myostatin-related muscle hypertrophy. The MSTN gene provides instructions for making a protein called myostatin, which is active in muscles used for movement (skeletal muscles) both before and after birth. In a much reviewed [3] academic research paper published in 2010 by the Journal of Musculoskeletal & Neuronal Interactions, Myostatin was proved to be the key factor linking muscle mass and bone structure.[4] This protein normally restrains muscle growth, ensuring that muscles do not grow too large. Mutations that reduce the production of functional myostatin lead to an overgrowth of muscle tissue. Myostatin-related muscle hypertrophy has a pattern of inheritance known as incomplete autosomal dominance. People with a mutation in both copies of the gene in each cell (homozygotes) have significantly increased muscle mass. People with a mutation in one copy of the MSTN gene in each cell (heterozygotes) also have increased muscle bulk but to a lesser degree.

The effect of this growth factor was first described in cattle as “bovine muscular hypertrophy” by the British farmer H. Culley in 1807. Cattle that have a myostatin gene deletion look unusually and excessively muscular.

Human-induced myostatin-related muscle hypertrophy

Researchers at Guangzhou Institutes of Biomedicine and Health in China have edited the genome of beagles to create double the amount of muscle.[5] Of the two beagles that were genetically modified, only one had increased muscle mass.[6] The ultimate aim of this project is to be able to better treat a genetic neuromuscular disease (Parkinson's disease).

Besides beagles, genetic modification has also been done in pigs[7] and fish.[8][9]

See also

References

  1. ↑ "Super Strong Kids May Hold Genetic Secrets" (in en). https://abcnews.go.com/Health/MedicineCuttingEdge/story?id=7231487&page=1. 
  2. ↑ "Lack of myostatin results in excessive muscle growth but impaired force generation". Proceedings of the National Academy of Sciences of the United States of America 104 (6): 1835–40. February 2007. doi:10.1073/pnas.0604893104. PMID 17267614. Bibcode: 2007PNAS..104.1835A. 
  3. ↑ "GDF 8 Myostatin Complete Profile, Dosage, Half-life, Mechanism of Action, Advantages and Disadvantages." (in en). https://steroidwiki.com/articles/hgh-peptides-articles/255-gdf-8-myostatin-complete-profile-dosage-half-life-mechanism-of-action-advantages-and-disadvantages.html. 
  4. ↑ Elkasrawy, M. N.; Hamrick, M. W. (2010). "Myostatin (GDF-8) as a key factor linking muscle mass and bone structure" (in en). Journal of Musculoskeletal & Neuronal Interactions 10 (1): 56–63. PMID 20190380. 
  5. ↑ "Scientists created the first genetically engineered dogs — and they are bizarrely muscular". Business Insider. 21 October 2015. https://www.businessinsider.com/scientists-edited-the-myostatin-gene-of-beagle-dogs-in-china-2015-10. 
  6. ↑ "Generation of gene-target dogs using CRISPR/Cas9 system". Journal of Molecular Cell Biology 7 (6): 580–3. December 2015. doi:10.1093/jmcb/mjv061. PMID 26459633. 
  7. ↑ "Super-muscly pigs created by small genetic tweak". Nature 523 (7558): 13–4. July 2015. doi:10.1038/523013a. PMID 26135425. Bibcode: 2015Natur.523...13C. 
  8. ↑ "Using CRISPR/Cas9-mediated gene editing to further explore growth and trade-off effects in myostatin-mutated F4 medaka (Oryzias latipes)". Scientific Reports 7 (1): 11435. September 2017. doi:10.1038/s41598-017-09966-9. PMID 28900124. Bibcode: 2017NatSR...711435Y. 
  9. ↑ "Targeted disruption of sp7 and myostatin with CRISPR-Cas9 results in severe bone defects and more muscular cells in common carp". Scientific Reports 6 (1): 22953. March 2016. doi:10.1038/srep22953. PMID 26976234. Bibcode: 2016NatSR...622953Z. 

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