Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation

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...

Arginase I enhances atherosclerotic plaque stabilization by inhibiting inflammation and promoting smooth muscle cell proliferation.

AIMS The aim of this study was to investigate the effect of Arginase I (ArgI) on plaque stabilization in unruptured atherosclerotic plaque and explore its mechanism. METHODS AND RESULTS The atherosclerotic plaque model was established in New Zealand rabbits by balloon injury of abdominal arteries and a high cholesterol (1%) diet. Arginase I overexpression reduced the content of macrophages an...

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...

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.