EBF1 controls an embryonic artery-forming niche that reactivates in pulmonary arterial hypertension

EBF1+ endothelial cells in the adult Aplnr+ gCap compartment reconstitute an embryonic artery-forming niche in pulmonary arterial hypertension, and gCap-specific Ebf1 overexpression drives severe disease.

• Why it matters: Developmental endothelial programs can be reactivated in adults to reshape vessels, but how an embryonic artery-forming niche returns and persists in PAH was unclear.
• What they did: The study mapped EBF1-defined ECs during embryogenesis and PAH, then tested function using gCap-specific Ebf1 overexpression in mice and gCap-specific Ebf1 deletion in mice plus endothelial-targeted AAV Ebf1 knockdown in rats.
• The result: Endothelial EBF1 is required for PAH pathogenesis: reactivation and persistence of EBF1+ ECs in occlusive intimal lesions is linked to neo-arterialization and occlusive remodeling, while Ebf1 loss protects in mice and rats.

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