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. 2025 Nov 21;18(1):1–21. doi: 10.1038/s44321-025-00344-x

Figure 1. Signaling pathways involved in vascular malformations.

Figure 1

Pharmacological inhibitors are indicated in boxes close to their respective targets. Crosses and lightning bolts denote components with loss-of-function and gain-of-function variants reported in vascular malformations, respectively. Sharp arrows indicate direct (solid line) or indirect (dashed line) activation. Blunt arrows show inhibition. ALK1 activin receptor-like kinase 1, ANG angiopoietin, AKT AK strain transforming, BMP9/10 bone morphogenetic protein 9/10, CCM cerebral cavernous malformation complex, EPHB4 Ephrin B4, ERK extracellular signal regulated kinase, IMiDs immunomodulatory drugs, MAPK mitogen-associated protein kinase, MEK mitogen-activated protein kinase kinase, MEKK3 mitogen-activated protein kinase kinase kinase 3, mTORC1/2 mammalian target of rapamycin complex 1/2, PI3Kα phosphoinositide 3 kinase α, PLCβ phospholipase Cβ, PTEN phosphatase and tensin homolog, RAF rapidly accelerated fibrosarcoma, RAS rat sarcoma viral oncogene homolog, RASA1 RAS p21 protein activator 1, RTK receptor-tyrosine kinase, SMAD4 mothers against decapentaplegic homolog 4, TGF-β transforming growth factor β, TIE2 tyrosine kinase with immunoglobulin and EGF homology domains, VEGFR vascular endothelial growth factor receptor.Created in BioRender. Galassi, I. (2025) https://BioRender.com/o21g614. Figure created with BioRender.com.