1064-184 Photodynamic therapy reduces atherosclerotic plaque inflammation, induces plaque stabilization and promotes plaque reduction

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...

Complement factor C5a induces atherosclerotic plaque disruptions

Complement factor C5a and its receptor C5aR are expressed in vulnerable atherosclerotic plaques; however, a causal relation between C5a and plaque rupture has not been established yet. Accelerated atherosclerosis was induced by placing vein grafts in male apoE(-/-) mice. After 24 days, when advanced plaques had developed, C5a or PBS was applied locally at the lesion site in a pluronic gel. Thre...

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...

The changing face of atherosclerotic plaque inflammation.