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lüll Endoglin in angiogenesis and vascular diseases ten Dijke P; Goumans MJ; Pardali EAngiogenesis 2008[]; 11 (1): 79-89Endoglin is a transmembrane auxillary receptor for transforming growth factor-beta (TGF-beta) that is predominantly expressed on proliferating endothelial cells. Endoglin deficient mice die during midgestation due to cardiovascular defects. Mutations in endoglin and activin receptor-like kinase 1 (ALK1), an endothelial specific TGF-beta type I receptor, have been linked to hereditary hemorrhagic telangiectasia (HHT), an autosomal dominant vascular dysplasia characterized by telangiectases and arteriovenous malformations. Endoglin heterozygote mice develop HHT-like vascular abnormalities, have impaired tumor and post-ischemic angiogenesis and demonstrate an endothelial nitric oxide synthase-dependent deterioration in the regulation of vascular tone. In pre-eclampsia, placenta-derived endoglin has been shown to be strongly upregulated and high levels of soluble endoglin are released into the circulation. Soluble endoglin was found to cooperate with a soluble form of vascular endothelial growth factor receptor 1 in the pathogenesis of pre-eclampsia by inducing endothelial cell dysfunction. Endoglin is highly expressed in tumor-associated endothelium, and endoglin antibodies have been successfully used to target activated endothelial cells and elicit anti-angiogenic effects in tumor mouse models. These exciting advances provide opportunities for the development of new therapies for diseases with vascular abnormalities.|Amino Acid Sequence[MESH]|Animals[MESH]|Antigens, CD/genetics/*physiology[MESH]|Endoglin[MESH]|Humans[MESH]|Intracellular Signaling Peptides and Proteins/*physiology[MESH]|Molecular Sequence Data[MESH]|Neovascularization, Pathologic/*metabolism/pathology[MESH]|Neovascularization, Physiologic/*physiology[MESH]|Receptors, Cell Surface/genetics/*physiology[MESH]|Vascular Diseases/*metabolism/pathology[MESH] |