Cell state · L2
FIB.adventitial.activated_remodelling
292 cells in the full atlas (not the displayed sample).
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Marker genes
ADAMTS4, ATP1B3, CTH, HAS1, MT1A, MT1M, NAMPT, NR4A1, NR4A2, NR4A3, RANBP2, RBKS, TIPARP, WT1, ZNF331
Annotation genes
ADAMTS4, HAS1, NAMPT, NR4A1
Annotation rationales
Adventitial fibroblasts sit at the vessel–stroma edge and are among the first stromal cells to sense hemodynamic and inflammatory shifts. Immediate-early nuclear receptors (NR4A1/2/3) switch on within minutes of TNF/IL-1/adrenergic signals, pushing a transient pro-resolving state. NAMPT fuels the NAD salvage pathway, sustaining redox and PARP/Sirtuin signaling during activation. Matrix editors (ADAMTS4) and HAS1 drive a hyaluronan-rich pericellular coat that hydrates tissue, spaces collagen, and binds chemokines. Metallothioneins (MT1A/MT1M) buffer Zn/ROS bursts that accompany vascular irritation. Together this is a rapid-on/rapid-off activation module tuned to microvascular stress.
Functional implications
Creates a deformable, HA-rich matrix “cushion” that absorbs pressure pulses, binds and titrates chemokines, and transiently loosens collagen to allow leukocyte passage. Supplies NAD/redox currency to survive and coordinate early repair; trims proteoglycans via ADAMTS4 to re-establish vessel adventitia architecture once the inflammatory spike subsides.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.