Researchers find reason why many vein grafts fail

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NIH intramural–led study uncovers biology behind improper graft remodeling

National Institutes of Health researchers have identified a biological pathway that contributes to the high rate of vein graft failure following bypass surgery. Using mouse models of bypass surgery, they showed that excess signaling via the Transforming Growth Factor Beta (TGF–Beta) family causes the inner walls of the vein to become too thick, slowing down or sometimes even blocking the blood flow that the graft was intended to restore. Inhibition of the TGF–B signaling pathway reduced overgrowth in the grafted veins.

The team, led by Manfred Boehm, M.D., chief of the Laboratory of Cardiovascular Regenerative Medicine at NIH’s National Heart, Lung, and Blood Institute, identified similar properties in samples of clogged human vein grafts, suggesting that select drugs might be used in reducing vein graft failure in humans.

Endothelial cells not only form the inner lining of a blood vessel, but also contribute to blood vessel narrowing as shown in this mouse vein graft model. Endothelial cells lose their typical morphology and become more like smooth muscle cells. This change in cellular properties indicates that endothelial–to–mesenchymal transition (EndMT) is operative in vein graft stenosis.

This study will be published March 12 in Science Translational Medicine.