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. 2022 Mar 1;2022:2924773. doi: 10.1155/2022/2924773

Figure 1.

Figure 1

Demonstrates mechanisms and different pathways by which galectins can participate in the pathological process of atheromatous plaque formation as well as the induction of endothelial injury within blood vessels. RhoA: Ras homolog family member A; ROCK: Rho-associated protein kinase; nFATc3: nuclear factor of activated T-cells cytoplasmic 3; LDL: low-density lipoprotein; PeNOS: phospho-endothelial nitric oxide synthase; ET-1: endothelin 1; IL-6: interleukin 6; CD36: cluster of differentiation 36; VSMC: vascular smooth muscle cells; ox-LDL: oxidized LDL; RAGE: receptor for advanced glycation end products; TNF: tumor necrosis factor; CCL 2/5/8: inflammatory chemokine ligands. This figure was created via BioRender (http://www.BioRender.com).