Key result
Bone marrow AT1aR disruption in mice reduces aortic atherosclerotic lesions and increases plaque stability.
Why the study?
Does disruption of AT1R in bone marrow reduce atherosclerosis in ApoE-/- mice?
Population
Apolipoprotein E-deficient (ApoE-/-) mice and bone marrow chimeric mice
Comparison
Genetic ablation or pharmacological blockade of… vs Mice with AT1aR-positive bone marrow
Design
Preclinical
Authors
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Suggests bone marrow AT1aR as atherosclerosis target; leaves open translation to clinical practice.
Does disruption of AT1R in bone marrow reduce atherosclerosis in ApoE-/- mice?
p-value: p=<0.05
Bone marrow AT1R plays a critical role in the pathogenesis and progression of atherosclerosis, highlighting a specific cellular mechanism for angiotensin II-mediated vascular disease.
Fukuda et al. (2007) studied Atherosclerosis. Disruption of bone marrow AT1aR vs. AT1aR-positive bone marrow was evaluated on Atherosclerotic lesions in aorta (p=<0.05). Disruption of bone marrow AT1aR in chimeric mice resulted in significantly less atherosclerotic lesions in the aorta (P<0.05) and more stable plaques compared to mice with AT1aR-positive bone marrow.
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