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. 2017 Nov 28;8:969. doi: 10.3389/fphys.2017.00969

Figure 1.

Figure 1

Proposed mechanisms by which PVAT modulates pathways linked to the pathogenesis of neointimal formation. Vascular injury induces inflammation in PVAT, which produces adipocytokines such as MCP-1, IL-6, and VCAM-1 and fosters recruitment of inflammatory cells (i.e., macrophages, neutrophils, T cells) into the vascular adventitia. Release of adipocytokines and chemokines, such as leptin and visfatin, from inflamed PVAT enhances phenotype switching of VSMCs, which proliferate and migrate to the neointima. Moreover, PVAT-medicated Angptl2 elevates MMP-2, and MCP-1 expression. PVAT-derived complement 3 induces adventitial fibroblast migration to neointima. VEGF released from PVAT also contributes to adventitial neovascularization. MCP-1, monocyte chemoattractant protein-1; IL-6, interleukin-6; VCAM-1; vascular cell adhesion molecule-1; VEGF, vascular endothelial growth factor; MMP-2, matrix metalloprotenease-2; VSMC, vascular smooth muscle cell; Angptl2, angiopoietin-like protein 2; C3, complement 3.