Table 2 Mechanism of the toxic effects of iodine contrast medium and the related ROS

Apoptosis

Oxidative stress induced by ROS is a potent inducer of apoptosis.

Ca²⁺ overload to ROS overproduction

p38 MAPK pathway, endothelin activation

[62]

Inhibiting Ca²⁺ overload

CaMII-mPTP pathway

[63]

Pyroptosis

Activate a strong inflammatory response.

Anti-inflammatory and antioxidant.

NLRP3-Caspase-1-GSDMD

[68]

ICM promote the release of inflammatory factors.

NLRP3-Caspase-1-GSDMD

[69]

Forming pores in cell membrane via GSDMD dissociation.

Caspase-4/5/11

[71]

Autophagy

Selective removal of damaged mitochondria, and protect cells from damage induced by excessive ROS.

Reducing mtROS and inhibiting the activation of the NLRP3 inflammasome to repair damaged mitochondria.

Pink1/Parkin pathway

[77]

Rapamycin enhancing mitophagy, alleviating mitochondrial damage and oxidative stress caused by ROS overproduction.

Up-regulating Parkin

[78]

Melatonin activated autophagy, repressed oxidative stress.

Inhibiting the NLRP3 inflammasome activation

[79]

3-MA inhibits autophagy

Enhances the oxidative stress

[80]

miRNAs

Regulate gene expression in the post-transcriptional level by degrading target mRNAs or inhibiting translation.

Overexpression of miR-188 promotes apoptosis of renal tubular epithelial cells.

SRSF7

[85]

miR-429 up-regulation inhibits the activation of the NF-ĸB pathway.

PDCD4

[86]

Overexpressed miR-30e-5p represses autophagy and promotes apoptosis

Beclin1

[87]

Upregulated miR-30c diminishes

pyroptosis can alleviates CI-AKI renal injury.

NLRP3

[88]