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Fig. 2 | Journal of Translational Medicine

Fig. 2

From: Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Fig. 2

Mechanism of CIN via complex pathways of ROS from in vitro and in vivo studies. Contrast media can generate ROS especially in high risk patients such as DM and CKD through 4 major pathways: (1) MAPK pathway including ERK, JNK and p38; (2) SIRT1 pathway including SIRT1, FoxO, NF-kB, PGC-1 and p53; (3) Rho/ROCK pathway including MYPT-1 and NF-kB; (4) Nrf-2/HO-1 pathway including Nrf-2, NQO1, GSH and HO-1. CIN, contrast-induced nephropathy; CKD, chronic kidney disease; DM, diabetes mellitus; ERK, extracellular signal-related kinases; FoxO, Forkhead-box transcription factor; GSH, glutathione; JNK, c-JUN N-terminal kinase; MAPK, mitogen-activated protein kinase; MYPT-1, myosin-phosphatase target unit; NF-kB, nuclear factor-kB; NQO1, nicotinamide adenine dinucleotide phosphate quinone oxidoreductase 1; Nrf-2/HO-1, nuclear factor erythroid 2-related factor 2/heme oxygenase 1; PGC-1, peroxisome proliferator-activated receptor gamma-assisted activating factor-1; ROCK, rho-kinase; ROS, reactive oxygen species; SIRT1, silent information regulator 1

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