The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Figure 4

Signaling pathways associated with CI-AKI and HGS in tubular epithelia contrast media trigger multiple signaling pathways in tubular epithelia, and the responses become more dynamic in HGS. The red circles show the pathways high-glucose status (HGS) caused directly, the blue boxes only show contrast-induced pathways, and the yellow rounded boxes give the common pathways which are likely to be the mechanisms firstly exist in diabetes mellitus (DM)/diabetes nephropathy (DN) and then worsen contrast-induced kidney injury (CI-AKI). The green dotted boxes contain substances or the target that may relieve CI-AKI. All the pathways pointed to apoptosis, inflammation, and fibrosis, which is the same like the former three figures. CREB, cAMP-responsive element binding protein; FoxO, forkhead boxO; HO-1, heme oxygenase-1; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; mTOR, mammalian target of rapamycin; NACA, N-acetylcysteine amide; NF-κB, necrosis factor-kappa B; Nrf2, nuclear factor-E2-related factor 2; P13K, phosphatidylinositol-3 kinase/serine-threonine kinase B; PKA/B/C, protein kinase A/B/C; SFN, sulforaphane; P, phosphorylation; NP, dephosphorylation.