Perivascular Mast Cells Promote Atherogenesis and Induce Plaque Destabilization in Apolipoprotein E–Deficient Mice
Key result
Activation of perivascular mast cells in apolipoprotein E-deficient mice promoted robust plaque expansion and destabilization, which was prevented by treatment with the mast cell stabilizer cromolyn.
Why the study?
Does mast cell activation promote atherogenesis and plaque destabilization, and can it be prevented by cromolyn in apolipoprotein E-deficient mice?
Population
Apolipoprotein E-deficient mice
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Mast cell stabilization should not yet change practice; hypothesis-generating for plaque stabilization in humans.
Structured PICO
Does mast cell activation promote atherogenesis and plaque destabilization, and can it be prevented by cromolyn in apolipoprotein E-deficient mice?
P
Population
Apolipoprotein E-deficient mice
I
Intervention
Systemic mast cell activation, targeted activation of perivascular mast cells, and treatment with the mast cell stabilizer cromolyn
O
Outcome
Plaque progression and destabilization (including intraplaque hemorrhage, macrophage apoptosis, vascular leakage, and leukocyte recruitment)surrogate
Mast cell activation promotes atherogenesis and plaque destabilization in vivo, suggesting that mast cell stabilization could be a novel therapeutic approach to prevent acute coronary syndromes.
Cite This Study
Bot et al. (2007) studied Atherosclerosis. Cromolyn was evaluated on Plaque progression and destabilization. Activation of perivascular mast cells in apolipoprotein E-deficient mice promoted robust plaque expansion and destabilization, which was prevented by treatment with the mast cell stabilizer cromolyn.