Cell state · L2
ASPC.niche_keeping_progenitor
3,504 cells in the full atlas (not the displayed sample).
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Marker genes
ALDH1A1, CFH, FBLN1, GGT5, IFITM1, IGFBP7, ITM2A, LTBP4, MYOC, OSR1, PTCH2, TFPI, TSPAN8, FOXS1, HHIP, HHIP-AS1, SUCNR1
Annotation genes
PTCH2, HHIP, FOXS1, LTBP4, FBLN1, OSR1, IGFBP7, TSPAN8, ALDH1A1, SUCNR1
Annotation rationales
Hedgehog axis (PTCH2, HHIP, FOXS1) marks a progenitor program typical of interstitial ASPCs; TGF-β/ECM niche coupling (LTBP4 sequesters latent TGF-β; FBLN1 ECM scaffolding) supports a stromal, non-adipocyte identity. Paracrine/vascular crosstalk genes (CFH complement regulation; TFPI anticoagulation) and metabolic priming (ALDH1A1 retinoid metabolism; SUCNR1 succinate sensing) indicate niche-sensing progenitors. Progenitor/stem features (OSR1 mesenchymal patterning, ITM2A stem-leaning, IGFBP7 growth-factor modulation, TSPAN8 motility/adhesion) and mechanosensing (MYOC) fit interstitial ASPCs. Absence of mature adipocyte markers (e.g., ADIPOQ, LEP, LPL) reinforces a preadipocyte/progenitor state; IFITM1/GGT5 reflect tissue-interface/stress readiness rather than terminal adipocyte function.
Functional implications
Niche-keeping progenitors that maintain the interstitial microenvironment, tune Hedgehog↔TGF-β signals to balance self-renewal vs preadipogenic commitment, and coordinate ECM remodeling and vascular–immune homeostasis (CFH/TFPI). Via SUCNR1 and ALDH1A1, they sense metabolic cues (succinate/retinoids) to gate differentiation; TSPAN8/IGFBP7/MYOC suggest migratory and mechanosensitive support of tissue remodeling, enabling rapid recruitment into adipogenesis or fibro-inflammatory repair after injury.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.