Front Immunol. 2026 Sep 29;17:1821747. doi: 10.3389/fimmu.2026.1821747. eCollection 2026.
ABSTRACT
Although reperfusion therapy improves the prognosis of acute myocardial infarction, myocardial ischemia-reperfusion injury continues to limit its clinical benefits, with neutrophil-driven inflammatory cascades representing a central mechanism of injury amplification. This article delineates the molecular event chain of neutrophils from recruitment to effector execution: activated neutrophils damage cardiomyocytes through three principal pathways-respiratory burst, degranulation, and neutrophil extracellular traps formation-thereby establishing a positive feedback loop that exacerbates inflammatory amplification. On this basis, we summarize therapeutic strategies targeting neutrophil migration, neutrophil extracellular traps formation, intracellular signaling pathways, mitochondrial homeostasis, immune phenotypes, and targeted drug delivery systems.
PMID:42819511 | PMC:PMC13624299 | DOI:10.3389/fimmu.2026.1821747