Direct or indirect endothelial cell transforming growth factor-β receptor activation initiates arteriolar hyalinosis

Jeremiah J Morrissey1

  • 1Division of Clinical and Translational Research, Department of Anesthesiology, School of Medicine, Washington University in St Louis, St Louis, Missouri 63110, USA. morrisse@wustl.edu

Kidney International
|September 29, 2012
PubMed

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.

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