Regression of cardiac hypertrophy by granulocyte colony-stimulating factor-stimulated interleukin-1β synthesis
Key result
Granulocyte colony-stimulating factor treatment significantly improved ejection fraction (70.48% vs 58.41%, P<0.001) and reduced cardiac fibrosis in mice after pressure unloading.
Why the study?
Does G-CSF treatment improve cardiac function and reduce fibrosis after pressure unloading in a mouse model of left ventricular hypertrophy?
Structured PICO
Does G-CSF treatment improve cardiac function and reduce fibrosis after pressure unloading in a mouse model of left ventricular hypertrophy?
P
Population
C57bl6 mice with left ventricular hypertrophy induced by transverse aortic constriction followed by debanding after 8 weeks.
I
Intervention
Granulocyte colony-stimulating factor (G-CSF) injection
C
Comparator
Saline injection
O
Outcome
Cardiac function (systolic and diastolic) and cardiac fibrosissurrogate
Main Result
Absolute Event Rate: 70.48% vs 58.41%
p-value: p=< 0.001
In a mouse model of aortic stenosis and pressure unloading, G-CSF treatment improved cardiac function and induced regression of myocardial fibrosis via IL-1β-mediated MMP expression.
Limitations
- Further basic research and clinical trials are required to prove beneficial effects in humans
Authors
Discussion
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Implication
G-CSF effects are hypothesis-generating in this mouse model; clinical translation requires prospective human studies.
Cite This Study
Szardien et al. (2011) studied Cardiac hypertrophy and fibrosis. Granulocyte colony-stimulating factor (G-CSF) vs. Saline injection was evaluated on Systolic function (ejection fraction) (p=< 0.001). Granulocyte colony-stimulating factor treatment significantly improved ejection fraction (70.48% vs 58.41%, P<0.001) and reduced cardiac fibrosis in mice after pressure unloading.