Hypoxia Stress Response
Gene co-expression module in Macrophages
| Category | Stress |
|---|---|
| Genes | 43 |
| Annotation certainty | 2 of 5 |
| Annotation consistency | 14 of 43 genes have a known function matching the annotation |
Why this annotation
Hub genes and the broader gene list point to a monocyte/macrophage tissue-resident and stress-adaptive program. STEAP3 (iron/endosomal reductase), ITGAM (CD11b, myeloid integrin), PDPN (podoplanin, tissue macrophage marker), CAVIN1 (caveolae biogenesis), TSC22D1 (glucocorticoid-responsive transcription factor), SPARC (ECM-associated secreted protein), BCAT1 (branched-chain amino acid catabolism, hypoxia/mTOR-linked), BNIP3 (hypoxia-induced mitophagy), NDRG1 (hypoxia/stress response), RCAN1 (calcineurin regulator, hypoxia/stress), THBD (thrombomodulin, anti-coagulant, tissue macrophage), BHLHE41 (circadian/tissue-resident macrophage TF), ECM1 and COL6A1 (ECM components), SLC39A8 (manganese/zinc transporter, inflammation-linked). The convergence of BNIP3, NDRG1, RCAN1, BCAT1, and BHLHE41 strongly suggests a hypoxia/metabolic stress program in tissue-resident monocyte-derived macrophages. All genes show weak membership and the module coherence is unknown, indicating a loosely co-regulated but biologically coherent stress-adaptive state. The mono_mac enrichment is consistent throughout. Neighbor context (M107 is a myeloid receptor/phagocytosis module) supports these being related myeloid programs.
Genes
ACE, AMPD3, APP, ASPH, BCAT1, BEX3, BHLHE41, BNIP3, CAPN2, CAVIN1, CCL18, COL6A1, COL6A2, CTSK, ECM1, ELK3, ENPP4, ERRFI1, FCGR2B, GPX3, IL7R, INSIG2, ITGAM, MMP12, MMP9, MYC, NDRG1, OPN3, PDPN, PSTPIP1, RCAN1, RHOU, RNASE1, SLC2A5, SLC39A8, SPARC, SPTAN1, STEAP3, TCEAL9, THBD, TLR2, TNNT1, TSC22D1
Most correlated modules
- Inflammatory Monocyte Activation · correlation 0.91
- Monocyte Phagocytic Identity · correlation 0.90
- SPP1 Tissue Remodeling · correlation 0.86
- Fc Receptor Phagocytosis · 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.