Role of iPLA2 on store operated Ca2+ entry (SOCE) and muscle force generation during aging
As we age, our muscles become weaker and smaller, a phenomenon known as sarcopenia. Calcium ions (Ca2+) are key signaling molecules in regulating muscle force, and the dysregulation of Ca2+in muscle is a significant contributor to sarcopenia. This study examines the hypothesis of a novel Ca2+ regulating pathway mediated by oxidized lipid, which is related to defective calcium homeostasis in aging muscles. The overall goal of this study is to increase our understanding in how the muscle Ca2+ is deteriorated by aging induced high oxidative stress, and also to determine how this abnormal processing of muscle calcium contributes to sarcopenia through a new Ca2+ regulating pathway that is related to lipid oxidation. This study will be the first to fully define the role of lipid oxidation in mediating muscle Ca2+ homeostasis, which is important for developing interventions for targeting muscle force generation in elderly in the future.
