Why the study?
The effects of S100A8/A9 blockade on myocardial inflammation and post-ischemic myocardial injury required investigation in a mouse model of coronary artery ligation.
Does S100A8/A9 blockade with ABR-238901 reduce neutrophil infiltration and myocardial infarction size in a mouse model of coronary artery ligation?
Population
Mouse model of coronary artery ligation
Comparison
3-day treatment with the S100A8/A9 blocker ABR-238901 vs control
Design
Preclinical animal study
Follow-up
3 days post-MI
Key result
A 3-day treatment with the S100A8/A9 blocker ABR-238901 significantly decreased neutrophil infiltration and reduced infarction size in a mouse model of myocardial infarction.
Authors
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Short-term S100A8/A9 blockade reduced infarct size and neutrophils in mice; leaves open immunomodulatory potential pending human translation.
Does S100A8/A9 blockade with ABR-238901 reduce neutrophil infiltration and myocardial infarction size in a mouse model of coronary artery ligation?
Short-term blockade of S100A8/A9 with ABR-238901 reduces acute neutrophil infiltration and infarct size in a mouse model of myocardial infarction, highlighting its potential as a therapeutic target to modulate post-ischemic inflammation.
Mareş et al. (2023) studied Myocardial infarction. ABR-238901 vs. Phosphate-buffered saline (PBS) was evaluated on Myocardial infarction size and neutrophil infiltration. A 3-day treatment with the S100A8/A9 blocker ABR-238901 significantly decreased neutrophil infiltration and reduced infarction size in a mouse model of myocardial infarction.