| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
Patients with mammalian target of rapamycin (mTOR)-inhibitor drug-eluting stent (DES) were reported to have impaired coronary endothelial function. There is no non-invasive biomarker of coronary endothelial dysfunction. Interleukin (IL)-1β is known to cause of endothelial dysfunction. We examined whether IL-1β were associated with coronary endothelial dysfunction after mTOR-inhibitor DES , and to investigate the possible mechanism.
Increased serum IL-1β could detect coronary endothelial dysfunction after DES implantation. mTOR inhibition triggers IL-1β release through transcriptional activation in CASMCs of stent site, which may lead to coronary endothelial dysfunction at distal to the stent.
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