Send to

Choose Destination
Trends Cardiovasc Med. 2011 Nov;21(8):229-33. doi: 10.1016/j.tcm.2012.05.016.

AIP1 in graft arteriosclerosis.

Author information

Interdepartmental Program in Vascular Biology and Therapeutics and the Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.


Graft arteriosclerosis (GA), the major cause of late cardiac allograft failure, is characterized by a diffuse, concentric arterial intimal hyperplasia composed of infiltrating host T cells, macrophages, and predominantly graft-derived smooth muscle-like cells that proliferate and elaborate extracellular matrix, resulting in luminal obstruction and allograft ischemia. Interferon-γ (IFN-γ), a proinflammatory cytokine produced by effector T cells, is a critical mediator for smooth muscle-like cell proliferation. We have exploited the power of mouse genetics to examine the function of AIP1, a signaling adaptor molecule involved in vascular inflammation, in two newly established IFN-γ-mediated models of GA. Our data suggest that AIP1 inhibits intimal formation in GA by downregulating IFN-γ-activated migratory and proliferative signaling pathways in smooth muscle-like cells.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center