Neutrophils play a dual role following myocardial infarction, exerting both detrimental effects through extracellular traps and vesicles, and beneficial pro-reparative effects in cardiac remodeling.
Neutrophils play a complex, dual role in post-myocardial infarction cardiac remodeling, exerting both detrimental inflammatory effects and beneficial reparative functions.
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.
Yonggang Ma (Fri,) conducted a review in Myocardial Infarction. Neutrophils play a dual role following myocardial infarction, exerting both detrimental effects through extracellular traps and vesicles, and beneficial pro-reparative effects in cardiac remodeling.
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