Targeting Rac1 for the prevention of atherosclerosis among U.S. Veterans with inflammatory bowel disease.

Q2 Biochemistry, Genetics and Molecular Biology Small GTPases Pub Date : 2022-01-01 DOI:10.1080/21541248.2021.1954863
S Scott Sutton, Joseph Magagnoli, Tammy H Cummings, James W Hardin
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引用次数: 1

Abstract

Evidence suggests that Ras-related C3 botulinum toxin substrate 1 (Rac1) might be a target in atherosclerotic disease (AD). We hypothesize that due to their ability to inhibit Rac1, thiopurines are associated with a lower risk of AD. We fit a time-dependent cox proportional hazards model estimating the hazard of AD among a national cohort of US veterans with inflammatory bowel disease. Patients exposed to thiopurines had a 7.5% lower risk of AD (HR = 0.925; 95% CI = (0.87-0.984)) compared to controls. The propensity score weighted analysis reveals thiopurine exposure reduces the risk of AD by 6.6% (HR = 0.934; 95% CI = (0.896-0.975)), compared to controls. Further exploration and evaluation of Rac1 inhibition as a target for AD is warranted.

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靶向Rac1预防美国炎症性肠病退伍军人动脉粥样硬化
有证据表明ras相关的C3肉毒毒素底物1 (Rac1)可能是动脉粥样硬化疾病(AD)的靶点。我们假设,由于它们抑制Rac1的能力,硫嘌呤与较低的AD风险有关。我们拟合了一个随时间变化的cox比例风险模型,估计患有炎症性肠病的美国退伍军人的AD风险。暴露于硫嘌呤的患者患AD的风险降低7.5% (HR = 0.925;95% CI =(0.87-0.984))。倾向性评分加权分析显示,硫嘌呤暴露使AD风险降低6.6% (HR = 0.934;95% CI =(0.896-0.975)),与对照组相比。进一步探索和评估Rac1抑制作为AD靶点是有必要的。
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来源期刊
Small GTPases
Small GTPases Biochemistry, Genetics and Molecular Biology-Biochemistry
CiteScore
6.10
自引率
0.00%
发文量
6
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