Limiting reductive stress for treating in-stent stenosis: the heart of the matter?

被引：9
作者：
de Haan, Judy B. [1 ]
机构：
[1] Baker IDI Heart & Diabet Inst, Diabet Complicat Div, Oxidat Stress Lab, Melbourne, Vic 3004, Australia
来源：
JOURNAL OF CLINICAL INVESTIGATION | 2014年 / 124卷 / 12期
关键词：
E-DEFICIENT MICE; CARDIOVASCULAR EVENTS; GLUTATHIONE; ATHEROSCLEROSIS; DISEASE; RISK;
D O I：
10.1172/JCI79423
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Restenosis after balloon angioplasty and stenting (BAS) remains an unsolved clinical dilemma for patients with coronary artery disease. A better understanding of the mechanisms that drive this phenomenon is likely to lead to more effective treatments. In this issue of the JCI, Ali et al. uncover a critical redox axis with the antioxidant enzyme glutathione peroxidase-1 (GPX1) at its hub and identify potential new therapeutic targets, such as ROS1 tyrosine kinase. This study represents a potential new approach to finding a treatment for BAS, with implications that may extend beyond BAS to other vasculopathies involving vascular remodeling.
引用
收藏
页码：5092 / 5094
页数：3
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