A single-cell transcriptome atlas reveals meniscal microenvironment variations during degeneration and cellular heterogeneity foundations of the inner–outer zone differences, suggesting novel cell subtypes as potential therapeutic targets.

Single-cell RNA sequencing to delineate the comprehensive postnatal RC enthesis growth from as early as postnatal day 1 to postnatal day 56.

Murine periosteum is highly enriched for osteoprogenitors, many of which express αSMA, but fracture callus chondrocytes are partially derived from other sources.

The molecular identity of bi-fated tendon-to-bone attachment cells, which display a mixture of transcriptomes of two neighboring cell types, enables the formation of the unique transitional tissue of the enthesis.

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.

NFATc1 is identified as a molecular marker of articular cartilage progenitor cells and a transcriptional repressor of chondrocyte differentiation, providing fundamental insights into the origin and differentiation mechanism of articular chondrocytes.

A single-nucleus atlas of bone repair uncovers the trajectories of periosteal skeletal stem/progenitor cells in response to fracture and identifies injury-induced fibrogenic cells as intermediate osteochondroprogenitors and key paracrine regulators.

The clonal oriented cell dynamics enables directional expansion and accurate scaling of sheet-like or rod-like cartilaginous elements and uncouples the mechanisms of elongation from thickness or diameter control.

The iPSCs derived from OA cartilage showed memory of disease which affect its chondrogenic potential and regulation at epigenetic and metabolic level may be used to control the regenerative potential of these iPSCs.

Fibro-adipogenic progenitors in skeletal muscle contribute to the neuromuscular pathogenesis of spinal muscular atrophy, and depletion of SMN in chondrocytes reduces local IGF sigaling in growth plate.