Cell state · L2
EC.venous.activated
3,509 cells in the full atlas (not the displayed sample).
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Marker genes
CCL2, CDKN1A, CSF3, ICAM1, IL6, PHLDA1, RCAN1, SELE, SOD2, TM4SF1
Annotation genes
CCL2, ICAM1, IL6, RCAN1, SELE
Annotation rationales
ICAM1/SELE enable leukocyte rolling and firm adhesion; CCL2/IL6/CSF3 drive monocyte, neutrophil, and systemic inflammatory recruitment. SOD2 provides mitochondrial ROS detox, while RCAN1 imposes calcineurin–NFAT braking, preventing overactivation. This combination typifies venous endothelial cells as first-line immune recruiters with built-in negative feedback.
Functional implications
Inflammation-engaged venous ECs that orchestrate immune cell extravasation, secrete cytokines to amplify leukocyte infiltration, and simultaneously apply intrinsic feedback (RCAN1/NFAT brake) to prevent vascular overactivation. Their role is to act as immune gateways while preserving venous wall integrity during chronic or systemic inflammation.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.