Laurent Metzinger
INSERM, France
Posters-Accepted Abstracts: J Nephrol Ther
Development of disease is often due to deregulation of gene expression. The gene program is controlled at the post-transcriptional level by the action of small non-coding RNAs known as microRNAs (miRNAs), short, single-stranded molecules that control mRNA stability or translational repression via base pairing with regions in the 3ΓΆΒ?Β? untranslated region of their target mRNAs. Over the last decade, considerable progress has been made to elucidate the roles of miRNAs in vascular pathogenesis and develop the use of miRNAs as innovative biomarkers in diagnostics, and as groundbreaking drugs in pharmacological treatments. We have recently shown that miR-223 is implicated in the course of chronic kidney disease (CKD) and is associated with vessel damage, such as vascular calcifications and atherosclerosis. This inflammatory miRNA is increased in vitro in vascular smooth muscle cells subjected to uremic toxins and is also increased in vivo in more advanced stages of CKD. Finally, miR-223 levels have been found to be deregulated in murine and human serum in the course of experimental CKD and in human diabetic patients. We are now in the process of evaluating its role in pre-clinical models of cardiovascular diseases, and are finding clues concerning its gene regulatory actions, using a combination of transcriptomics, proteomics and metabolomics. In conclusion, miR-223 could play a role in CKD vascular remodeling and may therefore represent an useful target to prevent or treat complications of CKD.
Email: laumet@u-picardie.fr
Journal of Nephrology & Therapeutics received 784 citations as per Google Scholar report