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While the specific mechanisms underlying endothelial dysfunction in CC may vary among the different pathological characteristics of MetS, but they converge on several common pathological pathways such as disturbances in both of the NO/Cyclic Guanosine Monophosphate (cGMP) and Ras homolog family member A (RhoA)/ Rho-associated coiled-coil containing protein kinase (ROCK) signaling pathways, imbalance of endothelium-derived vasoactive factors, alterations in sex hormone regulation, oxidative stress, and programmed cell death (Figure 1)