Cell state · L2
MUSC.activated_migratory
568 cells in the full atlas (not the displayed sample).
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Marker genes
APOD, CAV1, CCL2, CD74, CHRDL2, CXCL2, DLK1, FABP5, IFI27, IFITM3, IGFBP2, IGFBP7, PFN1, TAGLN, TAGLN2, TIMP1, TMSB10, TMSB4X
Annotation genes
CCL2, TAGLN, TIMP1, TMSB10, TMSB4X
Annotation rationales
Injury-proximal satellite cells flip on a motility/immune-alert program: TMSB4X/TMSB10 (G-actin shuttles) with PFN1 load actin for lamellipodia/filopodia; TAGLN/TAGLN2 stabilize actin–myosin bundles to generate traction across the basal lamina. Chemokines CCL2 (and CXCL2) recruit neutrophils/monocytes that clear necrotic fibers and deposit pro-regenerative cues. ECM regulators (TIMP1 balancing MMPs; CHRDL2 modulating BMP) tune stiffness/porosity so cells can infiltrate damaged endomysium. Antiviral/stress sentinels (IFI27, IFITM3) and lipid shuttles (FABP5, APOD) help cells traverse oxidized, lipid-rich damage zones. DLK1 can dampen Notch, nudging cells toward activation once they reach the lesion.
Functional implications
Rapidly home to myofiber breaks, pave migration tracts, and orchestrate the inflammatory milieu (via CCL2) to enable effective debridement. While moving, secrete matrix modulators (TIMP1) to prevent over-digestion, then dock onto injured fibers to prime myogenic entry and facilitate efficient fusion-driven repair.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.