The mechanisms of plaque rupture in acute coronary syndromes : Role of Oxidative stress and vasoactive factor

急性冠状动脉综合征斑块破裂的机制：氧化应激和血管活性因子的作用

• 批准号: 13670186
• 负责人: UEDA Makiko
• 金额: $ 2.18万
• 依托单位: Osaka City University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13670186/
• 关键词: Acute coronary syndrome; Plaque rupture; Oxidative stress; Oxidized LDL; Diabetes meilitus; neutrophil; プラーク破裂

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 ).

斑块破裂或侵蚀伴壁血栓形成被认为是导致稳定性冠状动脉病变转变为临床不稳定病变的最重要的形态学变化，从而导致急性冠状动脉综合征。然而，导致急性冠脉综合征的机制尚不清楚。我们先前已报道血管活性物质包括血管紧张素II和内皮素-1在人类冠状动脉粥样硬化的进展中起作用。在本研究中，我们证实了氧化低密度脂蛋白在糖尿病患者斑块不稳定的发生中的重要作用(糖尿病并发症杂志，16：60-，2002)。此外，我们还发现在急性冠脉综合征潜在的动脉粥样硬化斑块中存在明显的中性粒细胞，这表明中性粒细胞在调节人类动脉粥样硬化斑块的失稳中发挥了作用(循环106：2894-2900,2002)。

项目成果

Ehara S, Ueda M, Nanuko T, et al.: "Elevated Levels of Oxidized Low Density Lipoprotein Show a Positive Relationship With the Severity of Acute Coronary Syndromes"Circulation. 103(15). 1995-1960 (2001)

Ehara S、Ueda M、Nanuko T 等人：“氧化低密度脂蛋白水平升高显示与急性冠状动脉综合征的严重程度呈正相关”循环。

Fukunaga Y, Ueda M, et al.: "Thiazolidinediones, Peroxisome Proliferater-Activated Receptor-γ Agonists, Regulate Endothelial Cell Growth and Secretion of Vasoactive Peptides."Atherosclerosis. 158. 113-119 (2001)

Fukunaga Y、Ueda M 等人：“噻唑烷二酮类、过氧化物酶体增殖物激活受体-γ 激动剂，调节内皮细胞生长和血管活性肽的分泌。”动脉粥样硬化。

Naruko T, Ueda M, et al.: "Neutrophil infiltration of culprit lesions in acute coronary syndromes"Circulation. 106・23. 2894-2900 (2002)

Naruko T、Ueda M 等：“急性冠状动脉综合征中的中性粒细胞浸润”循环 106・23 2894-2900。

江原正一, 吉川純一, 上田真喜子: "Annual Review 循環器:高脂血症と冠動脈形態変化"中外医学社. 69-74 (2002)

Shoichi Ebara、Junichi Yoshikawa、Makiko Ueda：“心血管年度回顾：高脂血症和冠状动脉形态变化”Chugai Igakusha 69-74 (2002)。

Chen M., Ueda M, et al.: "Activation-Dependent Surface Expression of LOX-1 in Human Platelets"Biochem Biophys Res Commun. 282. 153-158 (2001)

Chen M.、Ueda M 等：“人类血小板中 LOX-1 的激活依赖性表面表达”Biochem Biophys Res Commun。