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Fig. 7 | Molecular Medicine

Fig. 7

From: AGEs promote atherosclerosis by increasing LDL transcytosis across endothelial cells via RAGE/NF-κB/Caveolin-1 pathway

Fig. 7

The mechanism of RAGE/NF-κB/Caveolin-1 pathway in AGEs-stimulated LDL transcytosis. Working model: the activation of the RAGE/NF-κB/Caveolin-1 axis plays a vital role in AGEs-promoted LDL transcytosis across ECs and development of AS. when exposed to AGEs, the RAGE-mediated NF-κB signaling is activated, which induces the expression of Caveolin-1, a main coat protein of caveolae and involved in LDL transcytosis in ECs. The downregulation of RAGE blocks NF-κB-RAGE-NF-κB signaling loop, resulting in a drop in Caveolin-1 expression and less LDL transcytosis, which ultimately delaying the development of AS. NF-κB nuclear factor kappa B, ECs endothelial cells, mRNA messenger ribonucleic acid, pri-RAGE primary transcript of RAGE, pri-Caveolin-1 primary transcript of Caveolin-1

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