Cross-Talk Between Muscle and Bone
Aging is associated with a progressive decline in muscle mass and function. Dysregulation of a set of cellular processes, such as low-grade inflammation, increased oxidative stress, reduced capacity of muscle regeneration, disrupted intracellular Ca2+ homeostasis, and altered lipid metabolism contribute to age-related muscle atrophy and muscle weakness, and are responsible for significant disability in older persons. To date, in attempting to determine the molecular components that lead to mass/strength decrements in the aged skeletal muscle, numerous studies using chromatography have screened or profiled biological signaling molecules such as proteins, hormones, bioactive lipids, antioxidants as well as other surrogate biochemical markers of muscle mass, which link to age-related skeletal muscle abnormalities. Accumulating evidence indicates that lipid mediators regulate skeletal muscle mass and function, and potentially influence muscle wasting, metabolism, and functional status in response to various pathological conditions. In this chapter, we attempt to provide an overview of the classification of lipid signaling mediators. We emphasize the biosynthesis, metabolism, and signaling pathways of AA-derived eicosanoids, which are involved in basic cellular process and thereby pathophysiological actions, particularly its association with bone-muscle crosstalk and skeletal muscle aging.
KeywordsBone-muscle crosstalk Aging Skeletal muscle Lipid mediator Cyclooxygenase pathway Lipoxygenase pathway Arachidonic acid-derived eicosanoids
This study was directly supported by NIH-NIA 2-P01 AG039355, 1-R01 AG056504, the George W. and Hazel M. Jay Endowment (to MB), and the UT System Science and Technology Acquisition and Retention Program (STARS) (to MB).
Conflict of Interest
No conflict of interest.
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