Smad2/Smad3 in endothelium is indispensable for vascular stability via S1PR1 and N-cadherin expressions
Transforming growth factor-beta (TGF-beta) is involved in vascular formation through activin receptor-like kinase (ALK)1 and ALK5. ALK5, which is expressed ubiquitously, phosphorylates Smad2 and Smad3, whereas endothelial cell (EC)-specific ALK1 activates Smad1 and Smad5. Because ALK5 kinase activity is required for ALK1 to transduce TGF-beta signaling via Smad1/5 in ECs, ALK5 knockout (KO) mice w