Macrophage MicroRNA-155 Promotes Cardiac Hypertrophy and Failure
Why the study?
Does genetic loss or pharmacological inhibition of microRNA-155 reduce cardiac inflammation, hypertrophy, and dysfunction in mice with pressure overload?
Population
Mice subjected to pressure overload and in vitro macrophage/cardiomyocyte models
Comparison
Genetic loss or pharmacological inhibition of… vs Wild-type mice
Design
Preclinical
Authors
Discussion
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Implication
miR-155 inhibition attenuates murine pressure-overload injury; hypothesis-generating for human HF therapy, pending clinical validation.
Structured PICO
Does genetic loss or pharmacological inhibition of microRNA-155 reduce cardiac inflammation, hypertrophy, and dysfunction in mice with pressure overload?
P
Population
Mice subjected to pressure overload (hypertensive heart disease model) and in vitro macrophage/cardiomyocyte models
I
Intervention
Genetic loss or pharmacological inhibition of microRNA-155
C
Comparator
Wild-type mice
O
Outcome
Cardiac inflammation, hypertrophy, and dysfunctionsurrogate
Inhibition of microRNA-155 reduces macrophage-dependent cardiac inflammation and hypertrophy in response to pressure overload in mice, highlighting a potential therapeutic target for heart failure.
Cite This Study
Heymans et al. (2013) studied this question.