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心肌缺血与糖尿病:氧化应激在心脏代谢与冠脉血流连接中的作用。

Myocardial Ischemia and Diabetes Mellitus: Role of Oxidative Stress in the Connection between Cardiac Metabolism and Coronary Blood Flow.

机构信息

Department of Cardiovascular, Respiratory, Nephrology, Anesthesiology and Geriatric Sciences, Sapienza University of Rome, 00161 Rome, Italy.

出版信息

J Diabetes Res. 2019 Apr 4;2019:9489826. doi: 10.1155/2019/9489826. eCollection 2019.

Abstract

Ischemic heart disease (IHD) has several risk factors, among which diabetes mellitus represents one of the most important. In diabetic patients, the pathophysiology of myocardial ischemia remains unclear yet: some have atherosclerotic plaque which obstructs coronary blood flow, others show myocardial ischemia due to coronary microvascular dysfunction in the absence of plaques in epicardial vessels. In the cross-talk between myocardial metabolism and coronary blood flow (CBF), ion channels have a main role, and, in diabetic patients, they are involved in the pathophysiology of IHD. The exposition to the different cardiovascular risk factors and the ischemic condition determine an imbalance of the redox state, defined as oxidative stress, which shows itself with oxidant accumulation and antioxidant deficiency. In particular, several products of myocardial metabolism, belonging to oxidative stress, may influence ion channel function, altering their capacity to modulate CBF, in response to myocardial metabolism, and predisposing to myocardial ischemia. For this reason, considering the role of oxidative and ion channels in the pathophysiology of myocardial ischemia, it is allowed to consider new therapeutic perspectives in the treatment of IHD.

摘要

缺血性心脏病(IHD)有几个危险因素,其中糖尿病是最重要的因素之一。在糖尿病患者中,心肌缺血的病理生理学仍不清楚:一些患者存在阻塞冠状动脉血流的动脉粥样硬化斑块,另一些患者则由于心外膜血管中没有斑块而出现冠状动脉微血管功能障碍导致心肌缺血。在心肌代谢和冠状动脉血流(CBF)的相互作用中,离子通道起着主要作用,而在糖尿病患者中,它们参与了 IHD 的病理生理学。暴露于不同的心血管危险因素和缺血状态会导致氧化还原状态失衡,定义为氧化应激,其表现为氧化剂积累和抗氧化剂缺乏。具体而言,属于氧化应激的几种心肌代谢产物可能会影响离子通道功能,改变它们调节 CBF 的能力,以响应心肌代谢,并易患心肌缺血。因此,鉴于氧化应激和离子通道在心肌缺血病理生理学中的作用,可以考虑在 IHD 的治疗中采用新的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a31/6476021/470cd688157d/JDR2019-9489826.001.jpg

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