Abstract
Transforming growth factor-beta (TGFβ) critically regulates the development of neointima formation following vascular injury; however the underlying signalling mechanisms remain to be fully elucidated. TGFβ signals via binding to specific cell surface type I (TβRI) and type II (TβRII) serine/threonine kinase receptor complexes and subsequently activates the canonical Smad signalling pathway, as well as other non-canonical signalling pathways. The two main TβRIs in vascular cells are ALK1 and ALK5. We aimed to perform detailed, mechanistic characterisation of the ALK1 and ALK5 TGFβ signalling pathways in the context of vein graft failure.
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