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. 2014 Nov 21;5:455. doi: 10.3389/fphys.2014.00455

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Copyright © 2014 Linden, Domschke, Erbel, Akhavanpoor, Katus and Gleissner.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Basic mechanisms of atherogenesis and studies specifically targeting inflammation in atherogenesis. Briefly, blood monocytes enter the subendothelial space where they differentiate toward macrophages and foam cells, which in turn secrete pro-inflammatory mediators leading to further inflammation, plaque growth and eventually plaque rupture. RECORD (rosiglitazone) and PROActive (pioglitazone) have studied the role of peroxysome proliferator-activated receptor-γ (PPARγ) agonists, which increase insulin sensitivity, glucose and free fatty acid (FFA) uptake, while reducing gluconeogenesis including anti-inflammatory effects. CANTOS (canakinumab) and CIRT (low dose methotrexate) target IL-1β or IL-6. ARISE (succinobucol), STABILITY and SOLID-TIMI52 (both darapladib) target oxidation of native LDL, which significantly contributes to foam cell formation. ILLUMINATE (torcetrapib), Dal-OUTCOMES (dalcetrapib) and REVEAL (anacetrapib) target HDL levels via inhibition of the cholesterol ester transfer protein (CETP), which is potentially atheroprotective. Red font: negative trial results; red-green font: partially positive results, substance abandoned for side effects; black font: results pending. CETP cholesterol transfer protein; FFA, free fatty acids; HDL, high density lipoprotein; IL, interleukin; LDL, low density lipoprotein; oxLDL, oxidized low density lipoprotein; PPAR, peroxysome proliferator-activated receptor; VLDL, very low density lipoprotein.