Venousization enables angiogenesis in the absence of VEGFR signalling.

Endothelial cells lacking VEGFR2 (Vegfr2 KO) still proliferate and ultimately contribute substantially to vascular networks in most organs by venousization, despite failing early sprouting.

• Why it matters: VEGF–VEGFR2 signalling is widely viewed as essential for angiogenesis, yet resistance to anti-VEGF therapies suggests endothelial adaptation mechanisms that remain unclear in vivo.
• What they did: Genetic mosaics were induced with iFlpMosaics and iSuRe-HadCre to track Vegfr2 KO endothelial cells across embryonic and postnatal development, alongside comparative single-cell RNA sequencing after acute versus long-term VEGFR2 loss.
• The result: Vegfr2 KO cells became dominant in veins, enabling later VEGF-independent angiogenesis; venousization and increased VEGFR1/VEGFR3 ligands were linked to adaptation, while NR2F2 loss significantly compromised Vegfr2 KO expansion.

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