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. 2023 Mar 14;13(3):427. doi: 10.3390/metabo13030427

Figure 3.

Figure 3

The link between IR and atherosclerosis; and potential genetic markers of IR and atherosclerosis. Hyperglycemia leads to IR, indicated by diminishing PI3K, Akt, eNOS, and NO bioavailability and production. IR causes ED, signified by increased oxidative stress and activation of protein kinase C and RAGE. Through inflammation, thrombosis, and vasoconstriction, ED brings about atherosclerosis and eventual CAD development. The relationship of genetic factors (gene polymorphisms and expression) highlighted ED in a central position among IR, CAD, atherosclerosis, and T2DM interplay. The associated genes are CHI3L1, CD36, LEPR, RETN, IL-18, RBP4, and RARRES2. Abbreviations: ↓, reduction; AKT, protein kinase B; CAD, coronary artery disease; CD36, cluster of differentiation 36; CHI3L1, chitinase-3 like-protein-1; ED, endothelial dysfunction; eNOS, endothelial nitric oxide synthase; IL-18, interleukin 18; IR, insulin resistance; LEPR: leptin receptor; PI3K, phosphoinositide 3-kinase; RAGE, the receptor for advanced glycation end products; RARRES2, retinoic acid receptor responder 2; RBP-4, retinol-binding protein 4; RETN, resistin.