Cell state · L2
CHOND.activated_fibro_like
3,395 cells in the full atlas (not the displayed sample).
These are the cell-population annotations shown in the SCREATE Cell Browser.
Read trait, study and gene evidence reports for this population →
Explore this population in Cell Browser →
Marker genes
ABRACL, IFITM2, IFITM3, LGALS1, LY6E, NME4, S100A4, TPM4, TUBB
Annotation genes
IFITM2, IFITM3, LGALS1, LY6E, S100A4
Annotation rationales
IFITM2/3 and LY6E denote an interferon-stimulated, antiviral/stress program that typically diverts resources away from anabolic ECM synthesis. S100A4 (fibroblast-like motility/EMT marker) and LGALS1 (galectin-1) point to cytoskeletal remodeling, adhesive reprogramming, and paracrine immunomodulation—features seen when articular chondrocytes acquire a fibro-chondrocyte–like state under inflammation or mechanical insult. The absence of strong matrix genes (e.g., COL2A1/ACAN) supports a catabolic, stress-adapted phenotype rather than matrix building.
Functional implications
Innate-defense, catabolism-leaning fibro-chondrocytes that prioritize antiviral/stress resistance over ECM anabolism. In the knee, they likely emerge in inflamed cartilage or at fissure margins, promoting pericellular matrix thinning, increased cell motility within damaged lacunae, and crosstalk with synovium via galectin-1. Functional outcome: reduced proteoglycan/collagen deposition, greater susceptibility to fibrillation, and contribution to OA-like degeneration under sustained cytokine load.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.