Research Paper Volume 13, Issue 2 pp 2553—2574

TLR2 regulates angiotensin II-induced vascular remodeling and EndMT through NF-κB signaling

Schematic illustration of the main findings. Ang II potentially engages TLR2 signaling pathway to activate NF-κB in vascular endothelial cells. NF-κB orchestrates the induction of EndMT transcription factors to reduce endothelial phenotype makeup and increase mesenchymal genes. In addition to regulating cell phenotype change, NF-κB increases the expression of extracellular matrix proteins. Ang II may cause the production and release of paracrine factors which may further facilitate EndMT in a TLR2-independent manner. Dotted lines indicate putative mechanisms where direct evidence of the underlying phenomenon is needed. These putative mechanisms include evidence that Ang II directly engages TLR2 and receptors or sensors involved in detecting and responding to Ang II-generated paracrine factors.

Figure 6. Schematic illustration of the main findings. Ang II potentially engages TLR2 signaling pathway to activate NF-κB in vascular endothelial cells. NF-κB orchestrates the induction of EndMT transcription factors to reduce endothelial phenotype makeup and increase mesenchymal genes. In addition to regulating cell phenotype change, NF-κB increases the expression of extracellular matrix proteins. Ang II may cause the production and release of paracrine factors which may further facilitate EndMT in a TLR2-independent manner. Dotted lines indicate putative mechanisms where direct evidence of the underlying phenomenon is needed. These putative mechanisms include evidence that Ang II directly engages TLR2 and receptors or sensors involved in detecting and responding to Ang II-generated paracrine factors.