Kyung Hee University · Medicine
Professor Weon Kim's research lab focuses on vascular biology and cardiovascular disease prevention, with a particular emphasis on identifying natural compounds and pharmacological agents that modulate endothelial function and vascular inflammation. The lab investigates the protective mechanisms of bioactive molecules such as curcumin, green tea catechins, and drugs like carvedilol and probucol in reducing oxidative stress, inhibiting inflammatory signaling pathways (e.g., NF-κB, JNK, STAT3), and preventing restenosis after stent implantation. Their work bridges molecular pharmacology with translational cardiology, aiming to develop novel therapeutic strategies for chronic smokers and patients at risk of atherosclerotic events.
Figures are computed from collected data and may differ slightly.
Curcumin, a yellow pigment of turmeric in curry, is reported to interfere with nuclear factor (NF)-kappaB. This study was designed to investigate the underlying pathway of antiinflammation of curcumin on endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with 10 ng/mL tumor necrosis factor (TNF)-alpha. Curcumin blocked the activation of NF-kappaB by TNF-alpha. Curcumin also reduced the intracellular reactive oxygen species (ROS), monocyte adhesion, phosphorylation
A short-term administration of green tea consumption induces a rapid improvement of EPC levels and FMD. Green tea consumption may be effective to prevent future cardiovascular events in chronic smokers.
Background The long-term clinical efficacy of intracoronary stenting is limited by restenosis and delivery by the stent of agents inhibiting cell cycle progression should prevent in-stent neointimal hyperplasia. Carvedilol is an antioxidant that inhibits smooth muscle cell proliferation and migration, whereas probucol is a vascular protectant and reduces stent restenosis by improving the lumen dimension at the stent placement site. Methods and Results BiodivYsio® phosphorylcholine-coated stents
Soluble guanylate cyclase (sGC) has been suggested as a therapeutic target for cardiac ischemia-reperfusion (IR) injury. Until now, the molecular mechanism of BAY 60-2770, a sGC activator, in cardiac IR injury has not been assessed. To identify the cardioprotective effects of BAY 60-2770 in IR-injured rat hearts, IR injury was established by occlusion of LAD for 40 min and reperfusion for 7 days, and the effects of BAY 60-2770 on myocardial protection were assessed by echocardiography and TTC st
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