The Effect Of Insufficient Production Of Dystrophin

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The contractile unit of a muscle cell is the sarcomere. Sarcomeres are mostly comprised of actin and myosin which pull and slide upon each other. These contractile units are linked end to end, like a chain, throughout the length of any given muscle. Certain proteins link the ends of these chains to the cell membrane. When a normally healthy individual exercises, some of these fibers, both in the sarcomere and at the connections to the cell wall, will be broken down due to damage (Leyva, 2013). Associated with this process includes the rebuilding of these fibers, in which the body builds back what was damaged stronger than before the damage occurred (Leyva, 2013). One of these end proteins is dystrophin. The purpose of this paper is to explore the implications of insufficient production of dystrophin, as in DMD.
Duchenne Muscular Dystrophy (DMD) is an X-linked genetic disorder in which muscle cells do not reproduce dystrophin. This means that during the rebuilding of new muscle, the muscles of those individuals who have MD do not appropriately repair and rebuild the fibers containing dystrophin. In essence, it is similar to a minor tendon tear on a microscopic level happening on the inside of the muscle. Due to this dysfunctional rebuilding of these connective components, there is an even greater discrepancy between the amount of force the sarcomeres can produce and the amount of force the fibers which connect to the cell membrane can withstand. This causes more

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