Fig. 2.

A schematic illustration of CAS pathogenesis including endothelial dysfunction, VSMC hyperreactivity, and adventitial/perivascular adipose tissue inflammation. CaM, calmodulin; EC, endothelial cell; ERS, endoplasmic reticulum stress; ET-1, endothelin-1; MLC, myosin light chain; MLCK, MLC kinase; NO, nitric oxide; ox-LDL, oxidized low-density lipoprotein; PKC, protein kinase C; PLC, phospholipase C; RhoA, Ras homolog gene member A; RhoGEF, Rho guanine nucleotide exchange factors; RhoK, Rho kinase; ROS, reactive oxygen species; VSMC, vascular smooth muscle cell.