During an ST-elevation myocardial infarction (STEMI), the myocardium undergoes a prolonged period of ischaemia. Reperfusion therapy is essential to minimize cardiac injury but can paradoxically cause further damage. Experimental procedures to limit ischaemia and reperfusion (IR) injury have tended to focus on the cardiomyocytes since they are crucial for cardiac function. However, there is increasing evidence that non-cardiomyocyte resident cells in the heart (as discussed in a separate review in this Spotlight series) as well as circulating cells and factors play important roles in this pathology. For example, erythrocytes, in addition to their main oxygen-ferrying role, can protect the heart from IR injury via the export of nitric oxide bioactivity. Platelets are well-known to be involved in haemostasis and thrombosis, but beyond these roles, they secrete numerous factors including sphingosine-1 phosphate (S1P), platelet activating factor, and cytokines that can all strongly influence the development of IR injury. This is particularly relevant given that most STEMI patients receive at least one type of platelet inhibitor. Moreover, there are large numbers of circulating vesicles in the blood, including microvesicles and exosomes, which can exert both beneficial and detrimental effects on IR injury. Some of these effects are mediated by the transfer of microRNA (miRNA) to the heart. Synthetic miRNA molecules may offer an alternative approach to limiting the response to IR injury. We discuss these and other circulating factors, focussing on potential therapeutic targets relevant to IR injury. Given the prevalence of comorbidities such as diabetes in the target patient population, their influence will also be discussed. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.

中文翻译：

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急性心脏保护中的循环血细胞和细胞外囊泡。

在ST抬高型心肌梗塞（STEMI）中，心肌经历长时间的局部缺血。再灌注疗法对于最大程度地减少心脏损伤至关重要，但可能自相矛盾地造成进一步的损害。限制局部缺血和再灌注（IR）损伤的实验程序往往集中在心肌细胞上，因为它们对心脏功能至关重要。但是，越来越多的证据表明，心脏中的非心肌细胞驻留细胞（如本Spotlight系列文章的另一篇评论所述）以及循环细胞和因子在这种病理学中起着重要的作用。例如，红血球除了具有主要的载氧作用外，还可以通过输出一氧化氮的生物活性来保护心脏免受IR伤害。众所周知，血小板与止血和血栓形成有关，但这些作用之外，它们分泌许多因子，包括1磷酸鞘氨醇（S1P），血小板活化因子和细胞因子，这些因子都可以强烈影响IR损伤的发展。考虑到大多数STEMI患者接受至少一种血小板抑制剂，这一点尤其重要。此外，血液中有大量循环囊泡，包括微囊泡和外泌体，它们可以对IR损伤产生有益和有害的作用。这些作用中的一些是通过将microRNA（miRNA）转移到心脏来介导的。合成的miRNA分子可以提供一种替代方法来限制对IR损伤的反应。我们讨论了这些和其他循环因素，重点是与IR损伤相关的潜在治疗靶标。鉴于目标患者人群中合并症（例如糖尿病）的患病率，他们的影响也将被讨论。本文是《心血管研究热点》一书的一部分，标题为“超越心肌细胞的心脏保护”，并作为欧洲联盟（EU）-心脏保护技术合作组织（COST）行动CA16225讨论的一部分出现。