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A review of myocardial ischaemia/reperfusion injury: Pathophysiology, experimental models, biomarkers, genetics and pharmacological treatment
CELL BIOCHEMISTRY AND FUNCTION ( IF 3.6 ) Pub Date : 2020-09-06 , DOI: 10.1002/cbf.3587
Mehmet Gunata 1 , Hakan Parlakpinar 1
Affiliation  

Cardiovascular diseases are known to be the most fatal diseases worldwide. Ischaemia/reperfusion (I/R) injury is at the centre of the pathology of the most common cardiovascular diseases. According to the World Health Organization estimates, ischaemic heart disease is the leading global cause of death, causing more than 9 million deaths in 2016. After cardiovascular events, thrombolysis, percutaneous transluminal coronary angioplasty or coronary bypass surgery are applied as treatment. However, after restoring coronary blood flow, myocardial I/R injury may occur. It is known that this damage occurs due to many pathophysiological mechanisms, especially increasing reactive oxygen types. Besides causing cardiomyocyte death through multiple mechanisms, it may be an important reason for affecting other cell types such as platelets, fibroblasts, endothelial and smooth muscle cells and immune cells. Also, polymorphonuclear leukocytes are associated with myocardial I/R damage during reperfusion. This damage may be insufficient in patients with co‐morbidity, as it is demonstrated that it can be prevented by various endogenous antioxidant systems. In this context, the resulting data suggest that optimal cardioprotection may require a combination of additional or synergistic multi‐target treatments. In this review, we discussed the pathophysiology, experimental models, biomarkers, treatment and its relationship with genetics in myocardial I/R injury.

中文翻译:

心肌缺血/再灌注损伤的回顾:病理生理学,实验模型,生物标志物,遗传学和药物治疗

心血管疾病是世界范围内最致命的疾病。缺血/再灌注(I / R)损伤是最常见的心血管疾病的病理学中心。根据世界卫生组织的估计,局部缺血性心脏病是全球主要的死亡原因,2016年导致900万人死亡。在发生心血管事件后,溶栓,经皮腔内冠状动脉成形术或冠状动脉搭桥手术被用作治疗方法。但是,恢复冠状动脉血流后,可能会发生心肌I / R损伤。众所周知,这种损害是由于许多病理生理机制而发生的,特别是活性氧类型的增加。除了通过多种机制导致心肌细胞死亡外,这可能是影响其他细胞类型(例如血小板,成纤维细胞,内皮细胞和平滑肌细胞以及免疫细胞。而且,多形核白细胞与再灌注过程中的心肌I / R损伤有关。对于合并症患者,这种损害可能不足,因为已证明可以通过各种内源性抗氧化剂系统预防这种损害。在这种情况下,所得数据表明最佳的心脏保护可能需要其他或协同的多靶点治疗的组合。在这篇综述中,我们讨论了心肌I / R损伤的病理生理学,实验模型,生物标志物,治疗及其与遗传学的关系。如证明的那样,可以通过各种内源性抗氧化剂体系来预防。在这种情况下,所得数据表明最佳的心脏保护可能需要其他或协同的多靶点治疗的组合。在这篇综述中,我们讨论了心肌I / R损伤的病理生理学,实验模型,生物标志物,治疗及其与遗传学的关系。如证明的那样,可以通过各种内源性抗氧化剂体系来预防。在这种情况下,所得数据表明最佳的心脏保护可能需要其他或协同的多靶点治疗的组合。在这篇综述中,我们讨论了心肌I / R损伤的病理生理学,实验模型,生物标志物,治疗及其与遗传学的关系。
更新日期:2020-09-06
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