TY - JOUR
T1 - Direct or indirect endothelial cell transforming growth factor-β receptor activation initiates arteriolar hyalinosis
AU - Morrissey, Jeremiah J.
N1 - Funding Information:
This work was supported by grant CA141521 from the National Cancer Institute, and by the Foundation for Barnes-Jewish Hospital.
PY - 2012/10/2
Y1 - 2012/10/2
N2 - Tacrolimus (FK-506) controls organ rejection; however, arteriolar hyalinosis is a frequent complication. By use of mice lacking FK-506-binding protein-12 in endothelial cells, Chiasson and co-workers explored the contribution of endothelial cells and the transforming growth factor-β pathway to define mechanisms of hyalinosis. Absence of this binding protein removed a tonic inhibition to activate the transforming growth factor-β system, causing arteriolar hyalinosis. However, tacrolimus can have effects on any biologic process involving receptors with a GS domain.
AB - Tacrolimus (FK-506) controls organ rejection; however, arteriolar hyalinosis is a frequent complication. By use of mice lacking FK-506-binding protein-12 in endothelial cells, Chiasson and co-workers explored the contribution of endothelial cells and the transforming growth factor-β pathway to define mechanisms of hyalinosis. Absence of this binding protein removed a tonic inhibition to activate the transforming growth factor-β system, causing arteriolar hyalinosis. However, tacrolimus can have effects on any biologic process involving receptors with a GS domain.
UR - http://www.scopus.com/inward/record.url?scp=84867032504&partnerID=8YFLogxK
U2 - 10.1038/ki.2012.178
DO - 10.1038/ki.2012.178
M3 - Comment/debate
C2 - 23018826
AN - SCOPUS:84867032504
SN - 0085-2538
VL - 82
SP - 838
EP - 839
JO - Kidney International
JF - Kidney International
IS - 8
ER -