Regulation of atherosclerotic plaque inflammation

The changing face of atherosclerotic plaque inflammation.

Sphingolipids Contribute to Human Atherosclerotic Plaque Inflammation.

OBJECTIVE Lipids are central to the development of atherosclerotic plaques. Specifically, which lipids are culprits remains controversial, and promising targets have failed in clinical studies. Sphingolipids are bioactive lipids present in atherosclerotic plaques, and they have been suggested to have both proatherogenic and antiatherogenic. However, the biological effects of these lipids remain...

Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation

Inflammation drives atherosclerotic plaque progression and rupture, and is a compelling therapeutic target. Consequently, attenuating inflammation by reducing local macrophage accumulation is an appealing approach. This can potentially be accomplished by either blocking blood monocyte recruitment to the plaque or increasing macrophage apoptosis and emigration. Because macrophage proliferation w...

lysophosphatidylcholine in Human Atherosclerotic Plaque inflammation

A rterial inflammation is the principal driving force responsible for atherosclerotic plaque development and destabilization. There is strong evidence that this inflammation is induced by the retention and oxidation of low-density lipo-protein (LDL) in the subendothelial space. Oxidized LDL is cytotoxic and may induce inflammation by causing arterial cell injury and by recruiting oxidized LDL-s...

Imaging atherosclerotic plaque inflammation with [18F]-fluorodeoxyglucose positron emission tomography.

BACKGROUND Atherosclerotic plaque rupture is usually a consequence of inflammatory cell activity within the plaque. Current imaging techniques provide anatomic data but no indication of plaque inflammation. The glucose analogue [18F]-fluorodeoxyglucose (18FDG) can be used to image inflammatory cell activity non-invasively by PET. In this study we tested whether 18FDG-PET imaging can identify in...