Department of Pathology, Northwestern University Feinberg School of Medicine, 300 East Superior St, Chicago, IL, 60611, USA.
Department of Pathology, Northwestern University Feinberg School of Medicine, 300 East Superior St, Chicago, IL, 60611, USA.
Curr Opin Pharmacol. 2022 Apr;63:102191. doi: 10.1016/j.coph.2022.102191. Epub 2022 Mar 8.
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.
免疫细胞的动员及其在血管外空间的积聚是组织损伤的一个关键后果。缺血组织再灌注后，免疫细胞的不当迁移和激活会加剧组织修复。在心肌梗死 (MI) 等缺血损伤后，PMN 是最早到达损伤部位的细胞，其反应对于缺血从炎症到消退再到组织修复的连续进展至关重要。然而，PMN 诱导的炎症也可能对心脏功能有害，并最终导致心力衰竭。在这篇综述中，我们强调了 PMN 在缺血性心力衰竭的关键细胞和分子事件中的作用。我们讨论了 PMN 代谢的新研究，以及这种代谢如何协调 PMN 的趋化、脱颗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。
