Hypoxia Response
Gene co-expression module in Fibroblasts
| Category | Stress |
|---|---|
| Genes | 17 |
| Annotation certainty | 4 of 5 |
| Annotation consistency | 9 of 17 genes have a known function matching the annotation |
Why this annotation
Hub genes include PLAU (urokinase plasminogen activator, inflammation/remodeling), HIF1A and EPAS1 (HIF1α and HIF2α, hypoxia transcription factors), ISG20 (interferon-stimulated gene), TGIF1 (TGF-β signaling), IL4R (cytokine receptor), NECTIN2 (cell adhesion), ACSL4 (lipid metabolism/ferroptosis), and TNFAIP8 (TNF-induced anti-apoptosis). The module is significantly upregulated in UC and CD inflammation and not reversed by treatment. The co-occurrence of HIF1A and EPAS1 as core hub genes strongly anchors this to hypoxia signaling, with PLAU, TGIF1, and IL4R reflecting downstream inflammatory-hypoxic crosstalk in fibroblasts. ACSL4 and TNFAIP8 are consistent with hypoxia-driven lipid and survival programs.
Genes
ACSL4, AP2S1, ARFGAP3, C4orf48, EPAS1, HIF1A, IL4R, ISG20, NECTIN2, PCNX1, PFDN2, PHC2, PLAU, SHC1, TGIF1, TNFAIP8, TOP1
Most correlated modules
- Inflammatory Fibroblast Activation · correlation 0.92
- NFAT-cAMP Signaling · correlation 0.89
- Proteasome Biogenesis · correlation 0.88
- AP-1 Inflammatory Stress · correlation 0.88
- Lysosomal Stress Response · correlation 0.87
- TGF-beta Fibrosis · correlation 0.86
- ER Stress UPR · correlation 0.85
- IL-1 Receptor Signaling · correlation 0.82
Module annotations were drafted by a large language model from the module's genes, then reviewed and approved by a domain expert. See sources & licences.