期刊
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
卷 10, 期 2, 页码 -出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a022210
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资金
- Netherlands CardioVascular Research Initiative
- Dutch Heart Foundation
- Dutch Federation of University Medical Centers
- Netherlands Organization for Health Research and Development
- Royal Netherlands Academy of Science
- LeDucq foundation
- TOP grant from the Netherlands Organization for Scientific Research (ZonMW-NWO)
Genetic studies in animals and humans indicate that gene mutations that functionally perturb transforming growth factor beta (TGF-beta) signaling are linked to specific hereditary vascular syndromes, including Osler-Rendu-Weber disease or hereditary hemorrhagic telangiectasia and Marfan syndrome. Disturbed TGF-beta signaling can also cause nonhereditary disorders like atherosclerosis and cardiac fibrosis. Accordingly, cell culture studies using endothelial cells or smooth muscle cells (SMCs), cultured alone or together in two-or three-dimensional cell culture assays, on plastic or embedded in matrix, have shown that TGF-beta has a pivotal effect on endothelial and SMC proliferation, differentiation, migration, tube formation, and sprouting. Moreover, TGF-beta can stimulate endothelial-to-mesenchymal transition, a process shown to be of key importance in heart valve cushion formation and in various pathological vascular processes. Here, we discuss the roles of TGF-beta in vasculogenesis, angiogenesis, and lymphangiogenesis and the deregulation of TGF-beta signaling in cardiovascular diseases.
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