chondrocytes

[Bone Research] Using metabolomics analysis and genetic in vivo models, the authors showed that maintaining intracellular serine homeostasis was essential for chondrocyte function.

[Nature Aging] Pharmacological inhibition of Stat3 activation or genetic ablation of Stat3 in chondrocytes reversed aberrant accumulation of Runx2 and ECM-degrading enzymes and limited osteoarthritis deteriorations caused by kindlin-2 deficiency.

[Cell Death & Disease] Androgens-androgen receptor (AR) signaling activated the AR/ARA55/FAK complex and induced the collagen-integrin α2β1 gene expression that was required for promoting the AR-mediated periosteum-derived progenitor cell migration.

[Bone Research] Expression and lineage analysis showed selective expression of discoidin domain receptor 2 (Ddr2) at early stages of bone formation in the resting zone and proliferating chondrocytes and periosteum.

[Journal of Tissue Engineering] Investigators used engineered cartilage microtissues formed from bone marrow-derived stromal cells or expanded articular chondrocytes to study the impact of enzyme treatment on cartilage tissue integration and matrix remodeling.

[Nature Communications] Scientists showed that matrix degradation and chondrocyte phagocytosis were mediated by fatty acid binding protein 5-expressing cells representing septoclasts, which had a mesenchymal origin and were not derived from hematopoietic cells.