Role of Neutrophils in Cardiac Injury and Repair Following Myocardial Infarction.
Neutrophils are first-line responders of the innate immune system. Following myocardial infarction (MI), neutrophils are quickly recruited to the ischemic region, where they initiate the inflammatory response, aiming at cleaning up dead cell debris. However, excessive accumulation and/or delayed removal of neutrophils are deleterious. Neutrophils can promote myocardial injury by releasing reactive oxygen species, granular components, and pro-inflammatory mediators. More recent studies have revealed that neutrophils are able to form extracellular traps (NETs) and produce extracellular vesicles (EVs) to aggravate inflammation and cardiac injury. On the contrary, there is growing evidence showing that neutrophils also exert anti-inflammatory, pro-angiogenic, and pro-reparative effects, thus facilitating inflammation resolution and cardiac repair. In this review, we summarize the current knowledge on neutrophils' detrimental roles, highlighting the role of recently recognized NETs and EVs, followed by a discussion of their beneficial effects and molecular mechanisms in post-MI cardiac remodeling. In addition, emerging concepts about neutrophil diversity and their modulation of adaptive immunity are discussed.
['Ma|Yonggang|Y|']
D056704:Adaptive Immunity D000818:Animals D016207:Cytokines D004195:Disease Models, Animal D065206:Extracellular Traps D000067128:Extracellular Vesicles D005786:Gene Expression Regulation D006801:Humans D018836:Inflammation Mediators D008264:Macrophages D051379:Mice D009203:Myocardial Infarction D009206:Myocardium D018919:Neovascularization, Physiologic D020556:Neutrophil Infiltration D009504:Neutrophils D017382:Reactive Oxygen Species
neutrophil myocardial infarction inflammation cardiac remodeling adaptive immunity angiogenesis macrophage