LCN2+ Astrocytes Mark a Pro-inflammatory Astrocyte State Associated with Secondary Brain Injury After Cerebral Venous Thrombosis

Lcn2-high reactive astrocytes are markedly enriched after cerebral venous thrombosis in a murine model, with late-stage trajectory localization and sustained inflammatory and stress gene upregulation.

• Why it matters: Even as acute mortality declines, the cellular mechanisms driving secondary brain injury and long-term dysfunction after CVT are unclear, limiting targeted therapies.
• What they did: The authors used single-cell RNA sequencing of murine CVT brain tissue, applied enrichment and pseudotime trajectory analyses, performed cell-cell communication inference, integrated cross-model data including MCAO, and tested function by genetic deletion of LCN2 in vivo.
• The result: LCN2 deletion alleviated CVT-induced brain tissue injury, supporting a detrimental role for the Lcn2-associated astrocyte state linked to inflammatory amplification, ferroptosis-related stress, and vascular-immune remodeling.

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