Can the Manipulation of Gene Expression Slow Muscle Atrophy?

As we advance in age, our muscles undergo atrophy, meaning they experience a reduction in strength and size. This is known as sarcopenia and is a natural occurrence in the aging process (Buford et al., 2010). Other factors such as diet, lack of physical activity, and disease can increase the rate of muscle atrophy (Buford et al., 2010). This is because increased muscle disuse increases the rate of protein degeneration past the rate of muscle synthesis (Hunter & Kandarian, 2004). Research also suggests that restricting the completion of the Akt growth pathway, a pathway involved in muscle growth, in muscles may further enhance muscle atrophy (Hunter & Kandarian, 2004). The Akt pathway utilizes kinases (proteins that transfer phosphate to other molecules) that are active during increased levels of protein synthesis but remain dephosphorylated during decreased levels of protein synthesis (Hunter & Kandarian, 2004). A recent study also suggests that muscle atrophy may be able to be directly manipulated by using specific proteins known as transcription regulators. Transcription regulators control a process called transcription, which is an ongoing process of making RNA from DNA; this RNA will then be used to make proteins in a process called translation. Research suggests that the removal of the expression of either 2 genes that code for these specific regulators results in the inhibition of decreased muscle size in mice (Hunter & Kandarian, 2004). The expression of these genes can be masked and unmasked by transcription regulators, resulting in the activation and deactivation of muscle atrophy. This mechanism of controlling gene expression is known as epigenetic, which involves manipulating gene expression without changing the genetic code of DNA. The expression of our genes is regulated in this way for many of our bodily processes. The epigenetic regulation of muscle atrophy could prove to be an important finding. Pharmaceuticals could be developed to promote these changes, and thus slow the degeneration of aging muscles. This could lead to a much easier transition into late adulthood considering that the loss of strength could prove detrimental to the way of life for most individuals. The generation of these drugs would be justified by the ethical value beneficence because we would be improving the livelihoods of others. It is also important to follow nonmaleficence so as to not promote a drug that could be harmful. Hopefully this study is the start of creating effective treatments to slow aging. References: Buford, T. W., Anton, S. D., Judge, A. R., Marzetti, E., Wohlgemuth, S. E., Carter, C. S., Leeuwenburgh, C., Pahor, M., & Manini, T. M. (2010). Models of accelerated sarcopenia: critical pieces for solving the puzzle of age-related muscle atrophy. Ageing research reviews, 9(4), 369–383. https://doi.org/10.1016/j.arr.2010.04.004 Hunter, R.B. & Kandarian, S.C. (2004). Disruption of either the Nfkb1 or the Bcl3 gene inhibits skeletal muscle atrophy. The Journal of Clinical Investigation, 114(10). doi.org/10.1172/JCI21696.