Figure 1.

Potential mechanism involved in the development of atherosclerosis. Atherosclerosis is a systemic disease that may involve multiple vessels, according to the stage of fibrosis and inflammation in the liver, there is a greater degree of progression of atherosclerosis. The transcriptional factor NF-κβ is the main responsible for generating proinflammatory cytokines, procoagulant and oxidative agents such as IL-6, CPR, TNF-α, PAI-1, ROS and the NLRP3 inflammasome that favors local recruitment of monocytes and, in smaller numbers, T lymphocytes into the endothelium in conjunction with oxLDL. In the intima, monocytes differentiate into macrophages and internalize oxLDL through scavenger receptors boosted by microRNA-155, subsequently transforming into foam cells. In turn, FGF are produced inducing smooth muscle proliferation forming a fibrous layer in the media layer. On the other hand, T lymphocytes arrive intima producing mediators such as IFNγ, which affects the ability of smooth muscle cells to produce interstitial collagen, causing instability in the layer. Furthermore, different pro-inflammatory cytokines inhibit the expression of different cholesterol transporters, mainly ABCA1 in foam cells by decreasing their cholesterol flow like microRNA-33 a/b and AGEs. NF-κβ, nuclear factor-κβ; IL-6, interleukin-6; CRP, C-reactive protein; TNF-α, tumor necrosis factor alpha; PAI-1, Plasminogen activator inhibitor-1; ROS, Reactive Oxygen Species; NLRP3, NOD-like receptor family, pyrin domain containing 3; oxLDL, oxidized low density lipoprotein; FGF, fibroblast growth factor; IFNγ, interferon gamma; ABCA1, ATP-binding cassette transporter A1; AGEs, advanced glycation end products; MMP, metalloproteinase; LXR, liver X receptor.