Disorders

Glycine activates MafG to upregulate glutathione metabolism and suppress chondrocyte ferroptosis in OA; novel metabolic protection pathway.

Metabolic reprogramming niche system halts OA progression by restoring chondrocyte energy metabolism and suppressing catabolic signaling.

Immunity-and-matrix-regulatory cells in engineered hydrogel promote hyaline-like cartilage regeneration, outperforming standard MSC approaches.

Hypertension accelerates OA progression through norepinephrine-driven neuroendocrine signaling that increases chondrocyte catabolic activity.

SESN2 promotes OA by inducing MFN2-dependent mitochondrial dysfunction in chondrocytes; SESN2 inhibition is chondroprotective.

Dual-modal antioxidant plus epigenetic synergy breaks the self-perpetuating OA cycle by targeting ROS and histone modification simultaneously.

Review: mitochondrial-ER stress crosstalk is an ageing-associated driver of OA chondrocyte death; convergent target for disease modification.

SIRT6 suppresses OA chondrocyte catabolism by deacetylating key transcription factors; SIRT6 loss accelerates cartilage breakdown.

Biphasic magnesium-based scaffold restores cartilage-subchondral bone metabolic balance; Mg2+ ion release promotes chondrocyte anabolism and suppresses bone resorption.

Fengshi Gutong capsule (traditional Chinese medicine) attenuates OA progression by targeting the PI3K/AKT/mTOR autophagy pathway in chondrocytes.

lncRNA MALAT1 regulates cholesterol-oxidative stress and iron homeostasis in chondrocytes; links lipid metabolism to ferroptosis in OA.

GAPDH-mediated glycolysis-senescence axis in OA chondrocytes: elevated GAPDH promotes aerobic glycolysis and SASP, driving chondrocyte aging.

Contemporary treatment algorithm for osteochondral lesions of the talus covering bone marrow stimulation, autologous chondrocyte implantation, and scaffold-based repair; highlights persistent challenges.

Reviews iron-dependent lipid peroxidation, ferroptosis, as a cell death route in OA chondrocytes.

Identifies a chondrocyte subpopulation with progenitor-like markers inside OA cartilage, a possible repair reservoir.

CRISPR/Cas9 deletion of a cartilage-specific FGFR3 enhancer normalized long bone and vertebral growth and reduced foramen magnum stenosis in mice.

IDH1/2 mutations in ~70 percent of conventional central chondrosarcomas drive D-2-hydroxyglutarate accumulation and epigenetic dysregulation; ivosidenib and enasidenib under investigation.

Integrated single-cell and experimental data link EIF6 and YWHAB to ROS production via p47phox-NOX2 under inflammatory conditions

Coordinated cell death explains why single-target inhibitors fail; natural products with pleiotropic action are proposed as strategy

PINK1 overexpression reduces senescence markers; mitophagy pathway as therapeutic target in OA

Critical overview of signaling interfaces driving hypertrophic and senescent chondrocyte phenotypes in OA

Review weighing local mechanical versus systemic metabolic and inflammatory drivers of OA; argues for a hybrid model.

m6A writer KIAA1429 silences USP3 to accelerate chondrocyte senescence and ferroptotic death in osteoarthritis.

AXL receptor tyrosine kinase signaling intersects with IDH1/2 mutation in chondrosarcoma; potential combined target.

Aging lowers the threshold for the hypertrophy-like shift (collagen X, MMP13 up) via senescence, oxidative stress, mitochondrial dysfunction, and epigenetic drift.

Review tying chondrocyte mechanism work to where OA treatment is actually headed.

Genomic and transcriptomic subgrouping of central chondrosarcoma; IDH mutation status is the primary molecular classifier.

FGFR3 gain-of-function mutation c.1138G>A (p.Gly380Arg) constitutively inhibits chondrocyte proliferation and differentiation; reviews targeted therapy landscape.