Abstract
Postoperative intimal hyperplasia is the major cause of the vein graft occlusion.
It is very important to establish an animal model for the start of research. After
my vascular surgery residency in Japan, I started my research work on postoperative
intimal hyperplasia at the University of Wisconsin-Madison. My research showed that
endothelial injury and monocyte infiltration is the key for postoperative intimal
hyperplasia, which is very similar to Ross' pathogenesis of atherosclerosis as an
inflammatory disease. Focusing on postoperative intimal hyperplasia as an inflammatory
disease, especially on tumor necrosis factor-α, FR-167653 (tumor necrosis factor-α
suppressive agent, inhibitor of p38 mitogen-activated protein kinase; Fujisawa Pharmaceutical Co., Ltd., Japan) is
found to suppress postoperative intimal hyperplasia in a rat model by reducing serum
monocyte chemoattractant protein-1 levels. However, FR-167653 is not commercially
available today. Because endothelial injury is the first step of postoperative intimal
hyperplasia, I investigated whether the free radical scavenger, edaravone (Radicut,
Mitsubishi Tanabe Pharma Co., Japan), which alleviates the endothelial injury in vitro, can also suppress postoperative intimal hyperplasia. Moreover, the free radical
scavenger edaravone (Radicut®, Mitsubishi Tanabe Pharma Co.) is also found to suppress
postoperative intimal hyperplasia, by alleviating endothelial injury. In clinical
settings, it is very important to detect postoperative intimal hyperplasia before
its establishment. Hepatocyte growth factor is not only a hepatic growth factor but
also a vascular endothelial growth factor. Recently, serum hepatocyte growth factor
level was found to be a candidate biomarker for postoperative intimal hyperplasia
in our rat model.
Keywords
postoperative intimal hyperplasia - endothelial injury - monocyte infiltration - monocyte
chemoattractant protein-1 - tumor necrosis factor-α suppressive agent - free radical
scavenger - hepatocyte growth factor