Signaling

Mechanotransduction modeled stoichiometrically under cyclical load; nitrogen availability is the primary constraint on matrix protein synthesis.

Chondrocytes and mesenchymal stromal cells (MSC) metabolism shapes cartilage matrix quality, but cartilage engineering lacks a non-destructive, time-resolved readout that links ...

Inflammation disrupts the normal metabolism of chondrocytes, shifting it toward catabolism and thereby accelerating cartilage extracellular matrix degradation

Osteoarthritis (OA) is a chronic and progressive joint disorder characterized by persistent inflammation, extracellular matrix (ECM) disruption, and chondrocyte apoptosis

Cyclodextrin-based metal-organic framework targeted to macrophages rescues efferocytosis and redox balance in the TMJ OA joint, promoting osteochondral repair; chondrocyte protection is downstream of macrophage polarisation.

Review arguing that mitochondrial dysfunction is a unifying mechanism across cartilage, bone, and muscle degeneration; frames mitochondrial quality control as a precision target for chondrocytes and other musculoskeletal cell types.

TGF-beta stabilizes Sox9 via p38 and Smad2/3; both pathways required independently. SOX9 protein level is a TGF-beta-dependent outcome.

Comprehensive review: Sox9, Runx2, Ihh, PTHrP, TGF-beta, BMP, FGF, and Wnt signaling in chondrocyte fate decisions from mesenchymal condensation through hypertrophy.

TGF-beta superfamily members show distinct expression profiles in chondral versus endochondral cartilage; Smad1/5/9 is the endochondral-specific branch.

Zone-intrinsic mechanotransduction confirmed: superficial and deep zone chondrocytes respond differently to the same oscillatory load.

Benninghoff arcade model confirmed at high resolution; tangential collagen orientation in superficial zone quantified.

Hypertrophic chondrocytes are a source of skeletal stem and progenitor cells, osteoblasts, and adipocytes; extends the 2014 lineage revision.

Shear stress from fluid flow is a key variable in bioreactor design; chondrocytes are highly sensitive to mechanosensation

Computational framework captures continuous mechanical interactions between chondrocytes and pericellular matrix under loading

Eight preHTC subtypes identified; CRIP1+ subtype is most expanded in OA weight-bearing regions; FN1 signaling elevated

Epigenetic axis DOT1L to ITCH to AURKA restrains matrix degradation in OA chondrocytes.

Glucocorticoid-induced methylation shuts off MALAT1, unleashing miR-124-3p to repress LPCAT3 and trigger ferroptosis in growth plate chondrocytes.

Engineering articular cartilage with hierarchical architecture and effective interfacial integration remains a major challenge

lncRNA OIP5-AS1 sequesters miR-223-3p, relieving FoxO3 repression and protecting chondrocytes from apoptosis in TMJ osteoarthritis; extends the lncRNA-sponge signaling pattern to a joint outside the knee.

Knee osteoarthritis (KOA) is a degenerative joint disease characterized by progressive cartilage degradation, synovial inflammation, and subchondral bone remodeling

Lactate accumulation in the OA joint drives lactylation of histone and non-histone proteins, shifting chondrocytes toward catabolic and senescent states and sustaining inflammation. A metabolic axis on top of the usual cytokine story.

Osteoarthritis (OA) is characterized by persistent inflammation, extracellular matrix (ECM) degradation, and impaired autophagy

Natural compound eugenol sustains ECM homeostasis in chondrocytes by balancing ALK1 and ALK5 arms of TGF-beta signaling.

scRNA-seq of 6 normal and 5 OA samples; superficial zone cells show highest catabolic protease and senescence gene expression

Plant lignan SDG reduces IL-1beta-driven inflammation in OA chondrocytes through ERBB2-coupled JAK2/STAT3 suppression.

Pararamosis, a tropical arthritis from ant venom, drives macrophage-to-chondrocyte IL-1beta signaling; model for studying cytokine-driven cartilage destruction.

Studies have shown that fluoride induces cartilage damage, however, the specific mechanism is unknown

N6-methyladenosine (m6A) plays a critical role in osteoarthritis (OA) pathogenesis

Dynamic monitoring of cell-matrix interfacial remodeling remains challenging with conventional endpoint assays, particularly in degeneration-relevant microenvironments

Urine-derived stem cells (USCs) represent an accessible and non-invasive cell source with reported chondrogenic differentiation potential

Chronic inflammatory signaling contributes to cartilage degeneration across multiple joint diseases, yet the molecular consequences of sustained cytokine exposure remain incompl...

Osteoarthritis (OA) involves extracellular matrix (ECM) degradation, inflammation, oxidative stress, mitochondrial dysfunction, and chondrocyte loss

Resting zone of the human growth plate holds subpopulations with quiescent stem cell features.

Although extracellular matrix (ECM) maturation during articular cartilage development is well recognized, quantitative, temporally resolved characterizations in large-animal mod...

Kashin-Beck disease (KBD) is a chronic, endemic osteoarticular disorder associated with T-2 toxin exposure, which is rapidly metabolized to HT-2 toxin in vivo

Osteoarthritis (OA) is a non-reversible degenerative disease characterized by progressive destruction of joint cartilage, formation of bone spurs, remodeling of subchondral bone...

Osteoarthritis (OA) is a degenerative musculoskeletal disease characterized by cartilage degradation and inflammation

Review of how compression is sensed and signalled by chondrocytes, and what that means for scaffold design.

Selenoprotein S (SelS) deficiency in chondrocytes activates Wnt/beta-catenin signaling and disrupts terminal differentiation; selenium deficiency linked to cartilage damage and osteoarticular disease; implicates SelS as a regulator of chondrocyte maturation via the Wnt pathway.

Review: physis integrates stem-like progenitor activity, clonal expansion, matrix remodeling, vascular invasion, and bone replacement

One of three 2014 lineage-tracing studies overturning apoptosis dogma; Col10a1-expressing hypertrophic chondrocytes contribute ~60 percent of mature osteoblasts.

Sox9 maintains chondrocyte fate; Runx2 drives hypertrophy; Ihh-PTHrP forms a feedback loop regulating the pace of hypertrophic differentiation.

Sox9 up-regulates PTHrP expression in association with Ihh/Gli2 signaling; the Ihh-PTHrP-Sox9 loop paces hypertrophic differentiation.