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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.

The regulation of bone homeostasis by the exercise-induced myokine irisin is in part potentiated by a direct action on osteoclast differentiation and resorption.

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

Loss or PTH1R-mediated repression of Zfp467 results in a pathway that increases Pth1r transcription via NFκB1 and thus cellular responsiveness to PTH/PTHrP, ultimately leading to enhanced bone formation.

Rgs12 protein is a novel regulator of the Nrf2 protein by facilitating the proteasomal degradation of the transcription factor during osteoclast differentiation.

Metabolic supplementation attenuates age-dependent declines in regeneration.

Adipsin, the oldest known adipokine, has a novel role as a a regulator of bone marrow fat and, consequently, overall bone health.

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.