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.
Frontiers in Immunology published a clinical update in Infectious Disease on 10 Apr 2026.
The item focuses on Stratified assessment of platelets in sepsis: from dynamic counts to functional phenotypes.
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