Key result
Elevated S100A12 exacerbates post-AMI injury via NETosis and correlates with higher 1-year mortality.
Why the study?
Does S100A12 promote NETosis and aggravate myocardial infarction injury via the Annexin A5-calcium axis?
Does S100A12 promote NETosis and aggravate myocardial infarction injury via the Annexin A5-calcium axis?
The S100A12-ANXA5-calcium influx axis promotes NETosis and exacerbates myocardial injury, representing a potential therapeutic target and biomarker for acute myocardial infarction.
Neutrophil extracellular traps (NETs) play a critical role in acute myocardial infarction (AMI) and the externalization of S100 family members. Here, we show the effects of S100A12 on NETs formation and myocardial injury following AMI. S100A12 expression increases rapidly in neutrophils and peaks on day 1 after AMI, promoting NETs production and exacerbating myocardial injury. DNase I, an inhibitor of NETs, reduces apoptosis of cardiomyocytes induced by S100A12. Mechanistically, the interaction of S100A12 and Annexin A5 (ANXA5) enhances calcium influx and promotes NETs formation. Blockage of ANXA5 effectively attenuates heart function impairment after AMI. Finally, we show that plasma S100A12 levels correlate with dsDNA concentration, and this correlation is associated with an increased risk of all-cause mortality during the 1-year follow-up of AMI patients. These findings, derived from male mice, reveal the S100A12-ANXA5-calcium influx axis as a potential therapeutic target and biomarker for AMI.
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Zhang et al. (2025) studied Acute myocardial infarction (AMI). S100A12 was evaluated on Myocardial injury, NETs formation, and all-cause mortality. S100A12 promotes NET formation and exacerbates myocardial injury via the Annexin A5-calcium axis, and its plasma levels correlate with increased 1-year all-cause mortality risk in AMI patients.
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