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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.

Glutamine deprivation reprograms chondrocytes, attenuates inflammation, and such intervention may be protective against joint inflammation.

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

Disruption of the intracellular vimentin network upon cellular stress results in enhanced cell surface vimentin on human osteoarthritic chondrocytes and might represent a novel membrane-associated marker of stress-induced premature senescence.

Alterations of DNA methylation were associated with articular cartilage degeneration in hemophilic arthropathy, and aberrant methylation and expression of TNXB promote blood-induced chondrocyte apoptosis by regulating AKT activation.

Modulation of division plane rotation in proliferating chondrocytes determines the ratio of clusters and columns, which may support the multifunctional design of the growth plate.

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.

Uncovering a new function of BMP signaling and enhancing our comprehension of the pathogenesis of microtia.

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.

Fibroblast growth factor induces dephosphorylation and inactivation of the NPR2 guanylyl cyclase, thus decreasing cyclic GMP production in growth plate chondrocytes and contributing to FGF-dependent decreases in bone growth.