Epigenetic profiling of femoral growth plate chondrocytes helps whittle-down GWAS height variants to fewer putative functional variants.

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.

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.

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.

Slow-cycling chondrocytes are maintained in a Wnt-inhibitory environment within the resting zone, unraveling a novel mechanism regulating maintenance and differentiation of parathyroid hormone-related protein (PTHrP)-expressing skeletal stem cells of the postnatal growth plate.

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.

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.

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

The application of different types of mechanical stimuli to chondrocytes, either by stretching the membrane or deflecting cell-substrate contacts, reveals that there are distinct but overlapping mechanoelectrical transduction pathways in these cells.

The transcriptomic and epigenetic landscapes of developing human articular and growth plate cartilage reveal putative gene regulatory networks governing lineage commitment and tissue homeostasis.