All muscle tissue has a similar overall function, the generation of force. However, the divergence of muscle types into skeletal, smooth, and cardiac classes has resulted in physiologically different cells that are specific to the tissue they serve. As a result the response to similar stimuli can often result in diverse physiological changes within muscle cells. Skeletal muscle atrophy and sarcopenia are conditions that involve the loss of skeletal muscle mass due to limb immobilization, bed rest, spaceflight, or aging. The loss of skeletal muscle is directly related to poor health outcomes during various additional disease states and is frequently cited as a comorbidity. However, in cardiac muscle poor outcomes are also achieved during states of excessive muscle growth (hypertrophy) which can result in poor cardiac tissue perfusion and ischemia. The purpose of my research is to investigate possible underlying mechanisms responsible for driving these two conditions (atrophy and hypertrophy) to determine if there are similar characteristics that lead to divergent outcomes in both muscle types. Despite these different pathologies, low oxygen (hypoxia) and reactive oxygen species (ROS) generation are frequently cited as occurring in both conditions. My research aims to determine the following:
- Identify how the different muscle cells behave when treated with known hypoxia related signaling molecules. These molecules have already been found to cause arterial smooth muscle contraction and relaxation by changing the function of the muscle cells. They have also been suggested to play a role in skeletal and cardiac muscles but the effects are not yet completely known.
- Determine the cellular signaling responsible for cardiac muscle growth. This research may be able to apply similar treatments to skeletal muscle cells to help alleviate conditions of skeletal muscle atrophy or sarcopenia.
Determine if the mechanism responsible for atrophy and sarcopenia in skeletal muscle. By determining this mechanism we can also assess whether pharmacological intervention is possible in cardiac tissue to alleviate some of the most symptoms associated with hypertrophy.