Metabolic stresses including hyperglycemia and hyperlipidemia mainly stimulate RhoA/ROCK activity via oxidative stress-dependent pathways and through activation of GEFs by tyrosine kinase and G-protein-coupled receptors; moreover, other protein kinases including adenosine monophosphate-activated protein kinase (AMPK) can activate RhoA (29–33, 76). Here, RHOA is linked to hyperlipidemia.