Key result
In a mouse model of pressure overload-induced heart failure, ICAM1 deficiency prevented left ventricular T-cell and monocyte infiltration, cardiac fibrosis, and systolic and diastolic dysfunction.
Why the study?
Does ICAM1 deficiency prevent pathological cardiac remodeling and dysfunction in a mouse model of pressure overload-induced heart failure?
Population
Mouse model of pressure overload-induced heart failure, including wild-type, ICAM1-deficient, and…
Comparison
ICAM1 deficiency (genetic knockout) vs Wild-type mice
Design
Preclinical
Authors
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ICAM1 may be a therapeutic target in pressure-overload HF; animal data leave open translation to patients.
Does ICAM1 deficiency prevent pathological cardiac remodeling and dysfunction in a mouse model of pressure overload-induced heart failure?
ICAM1 regulates pathological cardiac remodeling by mediating proinflammatory leukocyte infiltration, suggesting it as a potential therapeutic target for heart failure.
Salvador et al. (2016) studied Pressure overload-induced heart failure. ICAM1 deficiency vs. Wild-type mice was evaluated on Left ventricular leukocyte infiltration, cardiac remodeling, and function. In a mouse model of pressure overload-induced heart failure, ICAM1 deficiency prevented left ventricular T-cell and monocyte infiltration, cardiac fibrosis, and systolic and diastolic dysfunction.
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