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Our study demonstrates that both activation and deletion of the CB2 receptor do not relevantly modulate atherogenesis in mice.
Surprisingly, intimal lesion size did not differ between both groups in sections of the aortic roots and arches, suggesting that CB2 activation does not modulate atherogenesis in vivo.
In accord, i.p. application of the direct CB2 antagonist SR144528 in HCD-consuming ApoE−/− mice did not modulate atherogenesis in another report [27].
Similar(57)
Imbalance in the ratio of the T cell subgroups and inflammatory monocytes as well as in their effector cytokines can modulate atherogenesis and plaque composition in mice [36], [37].
Tumor necrosis factor- α stimulation together with obestatin treatment decreased vascular cell adhesion molecule-1 (VCAM-1) expression in endothelial cells cultures, suggesting that obestatin may modulate atherogenesis processes [ 8].
Endogenous mitochondrial oxidative stress is an important CVD risk factor that can modulate atherogenesis and cytokine-induced endothelial cell oxidant generation.
In summary, the present study made the novel observation that neither CB2 receptor stimulation nor its genetic deficiency modulates atherogenesis.
PPARγC161→T has a significant protective effect on atherogenesis in CAD and T2DM patients by modulating lipid metabolism.
The traffic-related particles enhanced atherogenesis in mice [6].
Classical atherogenesis in contrast probably plays a minor role here.
Selective blockade of the CB1 receptor inhibits atherogenesis in LDL receptor (LDLR -deficient mice [8].
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Justyna Jupowicz-Kozak
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