ArticleNature communications2026
Endogenous VEGF signaling acts as a guardian of human primed pluripotency.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
20 authors.
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Abstract
The maintenance of human embryonic stem cell (hESC) self-renewal and pluripotency is governed by distinct signaling pathways, yet endogenous pluripotency-supporting pathways remain understudied despite extensive exogenous signaling research. Here, we identify a previously unrecognized role of endogenous VEGF signaling in sustaining primed hESC pluripotency. VEGF signaling is robustly activated in primed hESCs, quiescent in naïve cells, and inactivated upon differentiation. Strikingly, targeted VEGFR inhibition (pharmacological, soluble decoy receptors [sFLT1/sKDR], or CRISPR-mediated VEGFR1/2 knockout) in primed hESCs disrupts self-renewal and induces trophoblast-like differentiation. Mechanistically, VEGFR inhibition activates the BMP pathway and down-regulates NANOG, which directly binds and represses select BMP components and trophoblast lineage-specific genes. Functionally, BMP inhibition partially and NANOG overexpression substantially rescue the phenotype induced by VEGF signaling ablation. Collectively, our work uncovers a pivotal VEGF-dependent network maintaining primed pluripotency, providing valuable insights into integrated pluripotency and lineage regulation by signaling cascades and transcription factors.
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