Key result
Blocking the CXCL12/CXCR4 axis with AMD3100 significantly reduced atrial fibrillation inducibility and duration in a mouse model by decreasing atrial inflammation and structural remodeling.
Why the study?
Atrial fibrillation is an increasingly prevalent arrhythmia with significant health and socioeconomic impact, but its underlying mechanism remains not well understood.
Does blocking the CXCL12/CXCR4 axis with AMD3100 reduce AF inducibility and structural remodeling in a mouse model of AF?
Does blocking the CXCL12/CXCR4 axis with AMD3100 reduce AF inducibility and structural remodeling in a mouse model of AF?
p-value: p=<0.05
The CXCL12/CXCR4 axis is upregulated in AF, and its antagonism with AMD3100 reduces AF inducibility and atrial remodeling in a preclinical model, suggesting a potential therapeutic target.
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Hypothesis-generating for CXCR4 blockade in AF; leaves open translation to human disease.
Liu et al. (2021) studied Atrial fibrillation (n=60). AMD3100 vs. Vehicle (normal saline) was evaluated on Atrial fibrillation inducibility and duration (p=<0.05). Blocking the CXCL12/CXCR4 axis with AMD3100 significantly reduced atrial fibrillation inducibility and duration in a mouse model by decreasing atrial inflammation and structural remodeling.
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