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激活转录因子3——心肌缺血再灌注损伤的内源性抑制剂(综述)

Activating transcription factor 3--an endogenous inhibitor of myocardial ischemia-reperfusion injury (Review).

作者信息

Yang Chao-Jun, Yang Jun, Fan Zhi-Xing, Yang Jian

机构信息

Department of Cardiology, The First College of Clinical Medical Sciences, Yichang, Hubei 443000, P.R. China.

出版信息

Mol Med Rep. 2016 Jan;13(1):9-12. doi: 10.3892/mmr.2015.4529. Epub 2015 Nov 6.

Abstract

Coronary heart diseases, particularly acute coronary syndrome, have increased in morbidity and mortality in recent decades. Percutaneous coronary intervention, coronary artery bypass grafting and thrombolytic agents are effective strategies to rescue the infarcted myocardium. In addition to acute myocardial infarction, the resulting myocardial ischemia‑reperfusion injury (MIRI) leads to serious secondary injury of the heart. Studies have demonstrated that activating transcription factor (ATF)/cyclic adenosine monophosphate response element binding family member ATF3 had a negative regulatory role in IRI, particularly in the kidney, cerebrum and liver. The present review expounded the expression characteristics of ATF3 and its protective effects against MIRI, providing a theoretical basis for the overexpression of ATF3 in the myocardium as a promising gene-therapeutic strategy for MIRI.

摘要

近几十年来,冠心病,尤其是急性冠脉综合征的发病率和死亡率有所上升。经皮冠状动脉介入治疗、冠状动脉旁路移植术和溶栓药物是挽救梗死心肌的有效策略。除急性心肌梗死外,由此导致的心肌缺血-再灌注损伤(MIRI)会导致心脏严重的继发性损伤。研究表明,激活转录因子(ATF)/环磷酸腺苷反应元件结合家族成员ATF3在缺血再灌注损伤中具有负性调节作用,尤其是在肾脏、大脑和肝脏中。本综述阐述了ATF3的表达特征及其对MIRI的保护作用,为心肌中ATF3的过表达作为一种有前景的MIRI基因治疗策略提供了理论依据。

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