Figure 9.

Proposed model of how FKBP11 affects the formation and progression of AAD. In response to environmental stress (such as Ang II), FKBP11 expression was induced in endothelium of the dissected aorta and it could provoke the pro-inflammatory state of the endothelial cells by interacting with NF-kB p65 subunit and promoting its nuclear translocation, and the produced pro-inflammatory cytokines further facilitated the circulating monocytes transmigrating through the endothelium to the middle layer of the aorta, where they differentiated into active macrophages and secreted MMPs and other ECM degrading proteins, finally promoted the formation and progression of aortic dissection.