| Project/Area Number |
13670186
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Osaka City University |
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Principal Investigator |
UEDA Makiko Osaka City University Graduate School of Medicine, Professor, 大学院・医学研究科, 教授 (10137193)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Acute coronary syndrome / Plaque rupture / Oxidative stress / Oxidized LDL / Diabetes meilitus / neutrophil / プラーク破裂 |
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| Research Abstract |
Plaque rupture or erosion with mural thrombus formation is considered to represent the most important morphological changes that underlie the transformation of stable coronary lesions into clinically unstable lesions, causing acute coronary syndromes. However, the mechanisms that cause acute coronary syndromes are still unclear.
We have previously reported that vasoactive substances including angiotensin II and endothelin-1 play a role in the progression of human coronary atherosclerosis. We have also shown that oxidative stress is a key factor in coronary atherogenesis.
In the present study, we have demonstrated an important role of oxidized low density lipoprotein in the genesis of plaque instability in patients with diabetes mellitus ( J Diabetes Complications 16 : 60 - 64, 2002 ). Moreover, we have shown the distinct presence of neutrophils in atherosclerotic plaques underlying acute coronary syndromes, suggesting that neutrophils play a role in mediating destabilization of human atherosclerotic plaques ( Circulation 106 : 2894-2900, 2002 ).
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