洞察心肌梗死的病理生理学

Basant Al-Botaty, Abeer El-Khoely, Elsayed Elsayed, A. Eissa
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引用次数: 2

摘要

作为非动脉粥样硬化的一种后果,缺血的影响主要是由于它是细胞死亡的主要前体。心肌细胞死亡可通过内在或外在途径触发。在这两种途径中,细胞凋亡已经通过不同的研究得到了明确的解释,但最近,坏死性下垂被确定参与其中。心脏的再生能力可以忽略不计,因此梗死区域是通过瘢痕形成取代死细胞来实现的。梗塞愈合是通过炎症级联反应触发的,由垂死细胞释放的警报引起。免疫细胞清除死细胞后,会激活成纤维细胞,促进细胞外基质蛋白的沉积。本文讨论了缺血后的事件,包括损伤、炎症和梗死心脏修复过程中的机械信号传导。此外,还介绍了心肌梗死可能出现的并发症,以及现有的治疗策略和一些新的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Insight into the Pathophysiology of Myocardial Infarction
as a of non-atherosclerotic Consequent effects of ischemia are primarily due to which is the main precursor of cell death. Myocardial cell death is triggered through intrinsic or extrinsic pathways. In both pathways, apoptosis has been clearly explained through different studies but recently, necroptosis was determined to be involved. The heart has negligible ability for regeneration, thus infarcted regions are by replacing dead cells with scar formation. Infarct healing is triggered through an inflammatory cascade, induced by alarmins released from dying cells. Clearance of dead cells by immune cells is followed with the activation of fibroblasts to promote deposition of extracellular matrix proteins. This discusses the events involved following ischemia including the mechanistic signalling during injury, inflammation, and repair of the infarcted heart. Moreover, the possible complications are mentioned along with the established treatment strategies and some new therapeutic approaches for myocardial infarction.
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