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

机译:限制治疗支架内狭窄的还原应力:问题的核心?

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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.
机译:球囊血管成形术和支架置入术 (BAS) 后的再狭窄仍然是冠状动脉疾病患者尚未解决的临床难题。更好地了解驱动这种现象的机制可能会导致更有效的治疗。在本期JCI中,Ali等人发现了一个关键的氧化还原轴,其中心是抗氧化酶谷胱甘肽过氧化物酶-1(GPX1),并确定了潜在的新治疗靶点,如ROS1酪氨酸激酶。这项研究代表了一种潜在的新方法来寻找 BAS 的治疗方法,其影响可能超出 BAS 扩展到其他涉及血管重塑的血管病。

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