Abstract
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.