Cell state · L2
ADIPO.hypoxia_remodelling
328 cells in the full atlas (not the displayed sample).
These are the cell-population annotations shown in the SCREATE Cell Browser.
Alternate spelling: ADIPO.hypoxia_remodeling. The atlas identifier uses “remodelling”.
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Marker genes
ABCC3, AMY2B, GPAM, HILPDA, HOXB8, LINC01230, LINC01632, RETSAT, RNPC3, TNS1
Annotation genes
ABCC3, AMY2B, GPAM, HILPDA, RETSAT, TNS1
Annotation rationales
Hypertrophic adipocytes frequently become oxygen-limited. HILPDA (a HIF target) promotes lipid-droplet growth and traps fatty acids in triglycerides, fitting a hypoxia-adaptation program. RETSAT (retinol saturase) and GPAM (rate-limiting TG synthesis) point to active lipid remodeling under stress. TNS1 (focal-adhesion/ECM) suggests extracellular-matrix reorganization as cells enlarge; ABCC3 (MRP3 transporter) is induced by HIF/oxidative stress to export organic anions and bile-acid–like metabolites, consistent with metabolite efflux under hypoxia. AMY2B could reflect trace exocrine contamination, but the core program matches hypoxia-responsive adipocytes remodeling the niche.
Functional implications
Adapt to low O₂ while preserving storage capacity. Increase TG synthesis and droplet stabilization (HILPDA, GPAM), shift retinoid/oxidative metabolism (RETSAT), and remodel focal adhesions/ECM (TNS1) to accommodate cell hypertrophy. Export potentially harmful metabolites (ABCC3). Paracrine outcome: pro-angiogenic and fibrotic cues that reshape the depot microenvironment.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.