{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T03:56:26Z","timestamp":1790740586907,"version":"4.1.0"},"reference-count":70,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Following acute myocardial infarction (AMI), neutrophils rush to the damaged heart tissue. Their presence is critical, and how they die influences whether the heart heals or suffers further injury. This outcome depends on specific cell death pathways of neutrophils, including NETosis, apoptosis, and autophagy. NETosis can be harmful when neutrophils release sticky, web-like structures (NETs) filled with toxic enzymes, particularly during early thromboinflammatory amplification. These webs trap platelets and trigger clotting, which blocks blood vessels and worsens heart damage. In contrast, timely neutrophil apoptosis is a quiet, controlled death that signals cleanup cells (macrophages) to remove debris and start tissue repair, although apoptotic signaling in other cardiac cell types or inappropriate time windows may be detrimental. Autophagy acts as a regulator, helping determine which of these paths the cell takes. Furthermore, platelets could modulate these specific cell death pathways by releasing soluble mediators (e.g., P-selectin, HMGB1, polyP, CXCL4), promoting NETosis while suppressing apoptosis to exacerbate ischemic myocardial injury. Some anti-inflammatory strategies could fail if broad immune suppression inadvertently disrupts reparative neutrophil apoptosis and efferocytosis. 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