Disorders

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.

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

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

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

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.

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

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

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

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

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