Why the study?
Whether Trem2 regulates macrophage polarization and improves ventricular remodeling via the JAK2/STAT3 pathway after acute myocardial infarction remains unclear.
Population
Mouse acute myocardial infarction model
Comparison
Myeloid-specific Trem2 knockout mice vs control mice, with sTREM2 supplementation and AG490 inhibition
Design
Preclinical animal and molecular study
Key result
Trem2 deficiency exacerbated ventricular remodeling and cardiac dysfunction post-AMI, whereas exogenous sTREM2 restored JAK2/STAT3 pathway activity and ameliorated cardiac function.
Authors
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May identify Trem2 as a post-MI HF target; hypothesis-generating and requires clinical validation before any practice change.
The Trem2-JAK2/STAT3 signaling axis regulates macrophage phenotypic switching and represents a promising therapeutic target for ameliorating post-AMI myocardial remodeling.
He et al. (2026) studied acute myocardial infarction. Trem2 deficiency (Mac-Trem2KO) and sTREM2 supplementation vs. Control mice was evaluated on ventricular remodeling and cardiac function. Trem2 deficiency exacerbated ventricular remodeling and cardiac dysfunction post-AMI, whereas exogenous sTREM2 restored JAK2/STAT3 pathway activity and ameliorated cardiac function.
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