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.

Chondrocytes derived from induced pluripotent stem cells with the dysplasia-causing TRPV4 mutations, V620I and T89I mutation, were resistant to BMP4-induced hypertrophy, suggesting a mechanism underlying the effects of TRPV4 dysfunction on the severity of skeletal dysplasia.

Cartilage cells transition through a proliferative intermediate to give rise to bone and marrow fat cells in long bones.

Membrane potential adjustment required for growth plate chondrocytic signal conversion from cGMP to Ca²⁺ influx toward long bone outgrowth.

MMP14 activity-mediated cleavage of the ectodomain of PTH1R modulates PTH signaling in the chondrocyte-derived osteoblast lineage, regulating osteogenesis and thereby bone metabolism, with therapeutic significance for bone-wasting diseases.

Integrated stress response-induced expression of ATF4 and its transactivation of SOX9 causes aberrant chondrocyte differentiation and skeletal defects which can be alleviated by modulating initiation-factor eIF2α phosphorylation translation control.

The principle underlying the appearance of the growth plate, an organ responsible for longitudinal growth, has implications for various cartilage pathologies including growth abnormalities in children, trauma and osteoarthritis.

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.

Corefucosylation contributes to the maintenance of the articular cartilage phenotype and depletion of FUT8 inhibits recovery from cartilage damage and promotes cartilage degeneration.

Cartilage and bone tumors arise from chondrocyte or osteoblast progenitors but not differentiated cells or multipotent mesenchymal stem cells (MSCs) via the IHH-Wnt/β-Catenin pathway.