Abstract

The intracellular mechanism of transforming growth factor- (TGF) signalling via kinase receptors and SMAD effectors is firmly established, but recent studies of human cardiovascular syndromes such as Marfan syndrome and pre-eclampsia have refocused attention on the importance of regulating the availability of active extracellular TGF. It seems that elastic extracellular matrix (ECM) components have a crucial role in controlling TGF signalling, while soluble and membrane bound forms of TGF co-receptors add further layers of regulation. Together, these extracellular interactions determine the final bioavailability of TGF to vascular cells, and dysregulation is associated with an increasing number of vascular pathologies.

Author affiliations

1. Molecular Cell Biology, Leiden University Medical Center, Postbus 9600, 2300 RC Leiden, The Netherlands.
   Email: p.ten_dijke@lumc.nl
2. Institute of Human Genetics, International Centre for Life, Central Parkway, Newcastle University, NE1 3BZ, UK.
   Email: helen.arthur@newcastle.ac.uk

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