This study investigates how NFAT transcription factors in platelets regulate immune and thrombotic responses during sepsis. Using the iNFATuation mouse model, the authors showed that platelet-specific inhibition of NFAT increases platelet aggregation, promotes neutrophil extracellular trap (NET) formation, and worsens outcomes in gram-negative septicemia.
NFAT inhibition in platelets leads to excessive aggregation and immune activation, exacerbating sepsis, and revealing a non-transcriptional regulatory role for NFAT in platelets.
iNFATuation mouse model with Cre-inducible expression of VIVIT peptide inserted into the Rosa26 locus using FLEx technology; activated in platelets via Pf4-Cre.
Sepsis, Platelet activation, NFAT signaling, Inflammation, NETs, Thrombosis
Knockin, Rosa26 locus, FLEx technology, Cre-inducible, Platelet-specific expression, VIVIT peptide
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