Immune cell mobilization and their accumulation in the extravascular space is a key consequence of tissue injury. Maladaptive trafficking and immune activation following reperfusion of ischemic tissue can exacerbate tissue repair. After ischemic injury such as myocardial infarction (MI), PMNs are the first cells to arrive at the sites of insult and their response is critical for the sequential progression of ischemia from inflammation to resolution and finally to tissue repair. However, PMN-induced inflammation can also be detrimental to cardiac function and ultimately lead to heart failure. In this review, we highlight the role of PMNs during key cellular and molecular events of ischemic heart failure. We address new research on PMN metabolism, and how this orchestrates diverse functions such as PMN chemotaxis, degranulation, and phagocytosis. Particular focus is given to PMN metabolism regulation by mitochondrial function and mTOR kinase activity.

免疫细胞动员及其在血管外空间的积累是组织损伤的关键后果。缺血组织再灌注后的适应不良运输和免疫激活会加剧组织修复。在心肌梗死 (MI) 等缺血性损伤后，PMN 是第一个到达损伤部位的细胞，它们的反应对于缺血从炎症到消退再到组织修复的顺序进展至关重要。然而，中性粒细胞引起的炎症也会损害心脏功能，并最终导致心力衰竭。在这篇综述中，我们强调了中性粒细胞在缺血性心力衰竭的关键细胞和分子事件中的作用。我们致力于对中性粒细胞代谢的新研究，以及它如何协调中性粒细胞趋化、脱粒和吞噬等多种功能。特别关注线粒体功能和 mTOR 激酶活性对 PMN 代谢的调节。