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Also, in the state of metabolic abnormalities, activated RhoA/ROCK pathway may also damage the endothelial function in CC through other pathways such as promoting the release of inflammatory factors and increasing the inflammatory response in vascular endothelial cells [38], as well as persistently impairing endothelial-dependent vasodilation to reduce endothelial NOS activation by inhibiting the insulin receptor substrate-1/phosphoinositide 3-kinase/protein kinase B pathway [39]