Unraveling the Role of Epicardial Adipose Tissue in Coronary Artery Disease: Partners in Crime?

Figures

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  Figure 1. Coronary artery disease progression. LDL, low-density lipoproteins; HDL, high-density lipoproteins; SMC, smooth muscle cells. The figure was produced using Servier Medical Art.

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  Figure 2. Search strategy flowchart. From the 571 abstracts collected in PubMed, using the keywords “epicardial adipose tissue and coronary artery disease”, 44 reports were used for the systematic review and 527 were excluded, according to the criteria above mentioned. CAD, coronary artery disease; EAT, epicardial adipose tissue.

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  Figure 3. The workflow for proteins/genes analysis using bioinformatic tools. SAT, subcutaneous adipose tissue.

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  Figure 4. Venn diagram representing the distribution of identified proteins per control evidencing the overlapped and unique proteins. Proteins identified in EAT from studies using EAT non-coronary artery disease (non-CAD) as control (A) and corresponding altered biological processes (C); Proteins identified in EAT from studies using SAT CAD as control (B) and corresponding altered biological processes (D).

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  Figure 5. Venn diagram representing the distribution of proteins per control evidencing the overlapped and unique proteins in EAT, using the protein up- and downregulated in EAT CAD as compared with EAT non-CAD and SAT CAD.

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  Figure 6. Interactions between EAT and atherosclerotic coronary arteries. In response to inflammatory cytokines released by atheroma, EAT can modulate the differentiation and function of adipocytes. EAT, located in close proximity with heart, can secrete adipocytokines which diffuse directly to the coronary arteries, promoting coronary inflammation. The figure was produced using BioRender and Servier Medical Art.