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S100A12 triggers NETosis to aggravate myocardial infarction injury via the Annexin A5-calcium axis
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S100A12 triggers NETosis to aggravate myocardial infarction injury via the Annexin A5-calcium axis
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Journal Article
S100A12 triggers NETosis to aggravate myocardial infarction injury via the Annexin A5-calcium axis
2025
Overview
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.
Neutrophil extracellular traps (NETs) contribute to heart damage after acute myocardial infarction (AMI). Here, the authors show that S100A12 promotes NETs formation and worsens injury, whereas blocking its interaction with ANXA5 reduces damage, suggesting a new therapeutic target for AMI.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/109
/ 13/2
/ 13/51
/ 13/89
/ 14/19
/ 14/63
/ 64/110
/ Animals
/ Calcium
/ Damage
/ Extracellular Traps - metabolism
/ Female
/ Humanities and Social Sciences
/ Humans
/ Injuries
/ Male
/ Mice
/ Myocardial Infarction - metabolism
/ Myocardial Infarction - mortality
/ Myocardial Infarction - pathology
/ Myocytes, Cardiac - metabolism
/ Myocytes, Cardiac - pathology
/ S100A12 Protein - metabolism
/ Science
