Skeletal muscle aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and regenerative capacity, which can lead to sarcopenia and increased mortality. Although the mechanisms underlying sarcopenia remain unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration. Therefore, identification of signaling pathways affecting satellite cell function during aging may provide insights into therapeutic targets for combating sarcopenia. Here, we show that a cell-autonomous loss in self-renewal occurs via alterations in fibroblast growth factor receptor-1, p38α and p38β mitogen-activated protein kinase signaling in satellite cells from aged mice. We further demonstrate that pharmacological manipulation of these pathways can ameliorate age-associated self-renewal defects. Thus, our data highlight an age-associated deregulation of a satellite cell homeostatic network and reveal potential therapeutic opportunities for the treatment of progressive muscle wasting.
Pubmed ID: 24531379 RIS Download
Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.
Digital microscopy software for research microscopy. It comes standard with drivers to control numerous instruments in and around the microscope. When online, data is acquired in a native-3D format over time, color and specimen locations in customizable experiment protocols. Data can be analyzed by a wide variety of tools for image processing including mathematical operations, statistics functions, analysis scripting and import to/export from MATLAB. Additional modules are available for special applications ranging from deconvolution to photomanipulation to multiphoton.
View all literature mentionsMus musculus with name C57BL/6J from IMSR.
View all literature mentions