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Título: | Controlling angiogenesis by two unique TGF-β type I receptor signaling pathways |
Fecha de publicación: | 2011 |
Editorial: | F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología. |
ISSN: | 1699-5848 0213-3911 |
Materias relacionadas: | 61 - Medicina |
Palabras clave: | Angiogenesis Pulmonary arterial hypertension |
Resumen: | Genetic studies in mice and humans have revealed a pivotal function for transforming growth factor-beta (TGF-β) in vascular development and maintenance of vascular homeostasis. Mice deficient for various TGF-β signaling components develop an embryonic lethality due to vascular defects. In patients, mutations in TGF-β receptors have been linked to vascular dysplasia like Hereditary Hemorrhagic Telangiectasia (HHT) and pulmonary arterial hypertension (PAH). Besides indirect effects by regulating the expression of angiogenic regulators, TGF-β also has potent direct effects on endothelial cell growth and migration, and we have proposed that TGF-β regulates the activation state of the endothelium via two opposing type I receptor/Smad pathways, activin receptor-like kinase (ALK)1 and ALK5. TGF-β is also critical for the differentiation of mural precursors into pericytes and smooth muscle cells. Furthermore, defective paracrine TGF-β signaling between endothelial and neighboring mural cells may be responsible for a leaky vessel phenotype that is characteristic of HHT. In this review, we discuss our current understanding of the TGF-β signaling pathway and its regulation of endothelial and vascular smooth muscle cell function. |
Autor/es principal/es: | Orlova, Valeria V. Liu, Zhen Goumans, Marie-José ten Dijke, Peter |
Forma parte de: | Histology and histopathology, Vol. 26, nº9 (2011) |
URI: | http://hdl.handle.net/10201/49414 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 12 |
Derechos: | info:eu-repo/semantics/openAccess |
Aparece en las colecciones: | Vol.26, nº9 (2011) |
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Orlova-26-1219-1230-2011.pdf | 759,31 kB | Adobe PDF | Visualizar/Abrir |
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