NDLI: Molecular Mechanisms of Renal Cellular Nephrotoxicity due to Radiocontrast Media

Content Provider	PubMed Central
Author	Michael, Ashour Faga, Teresa Pisani, Antonio Riccio, Eleonora Placido, Bramanti Sabbatini, Massimo Navarra, Michele Andreucci, Michele
Copyright Year	2014
Abstract	Modern iodinated radiocontrast media are all based on the triiodinated benzene ring with various chemical modifications having been made over the last few decades in order to reduce their toxicity. However, CIN remains a problem especially in patients with pre-existing renal failure. In vitro studies have demonstrated that all RCM are cytotoxic. RCM administration in vivo may lead to a decrease in renal medullary oxygenation leading to the generation of reactive oxygen species that may cause harmful effects to renal tissue. In addition, endothelin and adenosine release and decreased nitric oxide levels may worsen the hypoxic milieu. In vitro cell culture studies together with sparse in vivo rat model data have shown that important cell signalling pathways are affected by RCM. In particular, the prosurvival and proproliferative kinases Akt and ERK1/2 have been shown to be dephosphorylated (deactivated), whilst proinflammatory/cell death molecules such as the p38 and JNK kinases and the transcription factor NF- κ B may be activated by RCM, accompanied by activation of apoptotic mediators such as caspases. Increasing our knowledge of the mechanisms of RCM action may help to develop future therapies for CIN.
Related Links	http://dx.doi.org/10.1155/2014/249810
Starting Page	249810
File Format	PDF
ISSN	23146133
e-ISSN	23146141
Journal	BioMed Research International
Volume Number	2014
Language	English
Publisher	Hindawi Publishing Corporation
Publisher Date	2014-01-01
Access Restriction	Open
Rights Holder	Hindawi Publishing Corporation
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Microbiology Medicine Biochemistry, Genetics and Molecular Biology

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