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Aggravated restenosis and atherogenesis in ApoCIII transgenic mice but lack of protection in ApoCIII knockouts: the effect of authentic triglyceride-rich lipoproteins with and without ApoCIII

机译:ApoCIII转基因小鼠中的再狭窄和动脉粥样硬化加剧,但在ApoCIII基因敲除中缺乏保护:有或没有ApoCIII的纯正富含甘油三酸酯的脂蛋白的作用

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摘要

Aim Previously, our group and others have demonstrated a causative relationship between severe hypertriglyceridaemia and atherogenesis in mice. Furthermore, clinical investigations have shown high levels of plasma Apolipoprotein C-III (ApoCIII) associated with hypertriglyceridaemia and even cardiovascular disease. However, it remains unclear whether ApoCIII affects restenosis in vivo, and whether such an effect is mediated by ApoCIII alone, or in combination with hypertriglyceridaemia. We sought to investigate ApoCIII in restenosis and clarify how smooth muscle cells (SMCs) respond to authentic triglyceride-rich lipoproteins (TRLs) with or without ApoCIII (TRLs +/- ApoCIII).
机译:目的以前,我们的研究小组和其他研究人员已证明严重的高甘油三酯血症与小鼠动脉粥样硬化之间存在因果关系。此外,临床研究表明,血浆高载脂蛋白C-III(ApoCIII)水平与高甘油三酸酯血症甚至心血管疾病有关。但是,尚不清楚ApoCIII是否影响体内再狭窄,以及这种作用是否由单独的ApoCIII或与高甘油三酯血症联合引起。我们试图研究再狭窄中的ApoCIII,并阐明平滑肌细胞(SMC)对有或没有ApoCIII(TRLs +/- ApoCIII)的真实富含甘油三酸酯的脂蛋白(TRLs)的反应。

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