Stratified assessment of platelets in sepsis: from dynamic counts to functional phenotypes.

Sepsis is a major global cause of critical illness with high mortality. Sepsis-associated thrombocytopenia (SAT) is linked to markedly increased death risk and is a key indicator of poor prognosis. Although platelets are recognized as central players in the "inflammation-coagulation-immunity" network, most studies emphasize platelet counts rather than functional heterogeneity and underlying regulatory mechanisms, limiting the development of specific biomarkers and targeted therapies. Here, we characterize the "double-edged" role of platelets in sepsis. On the one hand, platelets recognize pathogens through pattern recognition receptors and exert anti-infective host defense functions; on the other hand, excessive platelet activation promotes endothelial injury and microthrombus formation through multiple signaling pathways and mediator release. These findings provide a concise framework linking platelet quantity, function, and mechanism in sepsis, and support the development of improved diagnostic and targeted treatment strategies.