Functional and molecular analyses of two distinct skeletal stem cell populations establish the important role of stem cell diversity that provides a framework for novel investigations into skeletal biology.

Hypertrophic chondrocytes of the growth plate undergo a process of dedifferentiation to generate marrow associated skeletal stem and progenitor cells (SSPCs), which ultimately re-differentiate into cells of the osteoblast or adipocyte lineages during skeletal development.

Skeletal muscle organoids differentiated from human pluripotent stem cells offer a system for investigating myogenesis and satellite cell development with translational potential for muscular dystrophy modeling and therapy development.

A set of ex vivo and in vivo experiments, including genetic ablation and regeneration studies, identify a key regulatory function of SOXF factors in muscle stem cells in mice.

Met and Cxcr4 signaling protects muscle stem cells from the noxious environment during acute inflammation.

Novel human iPS cell derived and primary skeletal muscle stem cells show that abnormal ACVR1 activation increases osteogenic/ECM gene expression and impairs myofiber repair, while revealing muscle-specific regenerative properties.

Building on previous work (Liu et al., 2015), it is shown that depletion or rescue of adult skeletal muscle stem cells is sufficient to induce or attenuate age-associated neuromuscular junction deterioration respectively.

Bulk and single-cell RNA-seq data demonstrated that muscle stem cells express low levels of canonical endothelial cell markers, including VEGFA receptors, and VEGFA-FLT1 pathway has a drastic effect on muscle stem cell survival through AKT1 in vitro and in vivo.

Using multiple genetic reporter system in human pluripotent stem cells, a transcriptional database for human early myogenesis has been established.

Myomaker is activated on muscle stem cells to promote their fusion with myofibers, which is essential for induction of pro-growth signaling pathways and physiological muscle hypertrophy.