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.

Meniscal Gli1+ cells are mesenchymal progenitors that contribute to the development and injury repair of meniscus.

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.

Parathyroid hormone attenuates osteoarthritis pain and joint degeneration by modification of subchondral bone remodeling and could be a potential disease-modifying therapy for osteoarthritis.

Hydrophilized graphene prevents protein denaturation at the air-water interface.

Single-cell combined spatial transcriptomics provides the molecular foundation for investigating how ligamental cell identities, biochemical functions, and interactions contributed to the ligamental degeneration process.

Down-regulation of GAS6 by M1 macrophages resulted in impaired efferocytosis for synovial apoptotic cells, causing synovial hyperplasia and obesity-associated OA development.

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

Osteoarthritis pathogenesis is driven by IgE-mediated mast cell activation.

In wild bonobos, sibling birth induced a sudden increase in urinary cortisol levels in the older offspring, a physiological response that occurred in all subjects and was independent of their age.