Skeletal muscle displays remarkable regenerative properties, with muscle-resident stem cells (satellite cells) the source of new myofibers following muscle injury. During homeostasis, satellite cells are in quiescence, a state maintained by multiple stem cell niche-derived signals. Such signals are produced by a variety of local cells, including the directly associated myofiber; vasculature-associated cells, including endothelial cells and pericytes; tissue-resident macrophages; and fibroadipogenic progenitor cells (FAPs). The basal lamina surrounding individual myofibers and the interstitial extracellular matrix between myofibers are important components of the satellite cell niche as well. Each of these cell types exist within their own supportive microenvironment. Upon injury, changes to the individual microenvironments of satellite cells and their niche cells drive productions of new signaling, matrix, and biomechanical cues, allowing orchestration of the complex interactions required for successful regeneration. In skeletal muscle diseases (such as the various muscular dystrophies) and in old age, the interactions between satellite cells and their niche, and niche cells with each other, are perturbed, contributing to pathology. Understanding the components and structures of the microenvironments that regulate muscle stem cells and their multitude of individual niche cells is an important goal for improving endogenous repair of muscle in aging and disease as well as for cell-based therapies.
We invite submissions that cover diverse aspects of satellite cells and their niche cells, including but not limited to:
- Signaling interactions that regulate satellite cell quiescence
- Changes to niche cell function during muscle regeneration after injury
- Perturbation of the microenvironment of satellite cells and various niche cells during aging and muscle disease
- Signaling and biomechanical cues in muscle homeostasis, regeneration, aging, and disease.
We encourage submissions that employ multidisciplinary approaches. Both original research and review articles are welcome.