Key result
C57BL/6 mice had a more pronounced and prolonged inflammatory response and higher mortality due to cardiac rupture following myocardial infarction compared with BALB/c mice.
Why the study?
It was unknown whether a predisposition toward a proinflammatory phenotype influences innate immune response dynamics, infarct healing, and cardiac rupture risk following myocardial infarction.
Does the genetic predisposition towards a proinflammatory phenotype (C57BL/6 vs BALB/c) influence the innate immune response and risk of cardiac rupture following myocardial infarction in mice?
Population
12–15-week-old male wild-type BALB/c and C57BL/6 mice
Comparison
C57BL/6 mice vs BALB/c mice
Design
Preclinical animal comparative study
Authors
Loading...
Genetic background should guide mouse MI model selection; leaves open translation to human rupture risk.
Does the genetic predisposition towards a proinflammatory phenotype (C57BL/6 vs BALB/c) influence the innate immune response and risk of cardiac rupture following myocardial infarction in mice?
C57BL/6 mice exhibit a more pronounced and prolonged inflammatory response post-myocardial infarction compared to BALB/c mice, leading to impaired repair and higher mortality from cardiac rupture.
Toor et al. (2019) studied Myocardial infarction. C57BL/6 mouse strain vs. BALB/c mouse strain was evaluated on Mortality due to cardiac rupture and inflammatory response dynamics. C57BL/6 mice had a more pronounced and prolonged inflammatory response and higher mortality due to cardiac rupture following myocardial infarction compared with BALB/c mice.