Home > Riviste > Minerva Medica > Fascicoli precedenti > Minerva Medica 2017 December;108(6) > Minerva Medica 2017 December;108(6):518-26

ULTIMO FASCICOLO
 

JOURNAL TOOLS

eTOC
Per abbonarsi
Sottometti un articolo
Segnala alla tua biblioteca
 

ARTICLE TOOLS

Publication history
Estratti
Permessi
Per citare questo articolo

 

REVIEW   

Minerva Medica 2017 December;108(6):518-26

DOI: 10.23736/S0026-4806.17.05395-2

Copyright © 2017 EDIZIONI MINERVA MEDICA

lingua: Inglese

Post-transcriptional regulation of cytokine in the context of renal inflammation

Eva FEIGERLOVÁ 1, 2, 3, 4 , Shyue-Fang BATTAGLIA-HSU 1

1 INSERM U954, Nutrition Génétique et Exposition aux Risques Environnementaux, Medical Faculty, University of Lorraine and Regional University Hospital Center of Nancy, Vandœuvre les Nancy, France; 2 Unit of Endocrinology, CHU de Poitiers, Pole DUNE, Poitiers, France; 3 Poitiers University, UFR Médecine Pharmacie, Poitiers, France; 4 INSERM, CIC 1402 & U1082, Poitiers, France


PDF


Mechanisms that control mammalian gene expression, notably mRNA stability and translation, have major functions in the modulation of the cellular response to internal and external stimuli. Altered posttranscriptional regulation of gene expression has been associated with many diseases. Such types of deregulation have also recently been noted on the inflammatory cytokines pertinent to kidney inflammation. In this article, we summarize briefly the recent knowledge obtained from both human and experimental systems on the details of posttranscriptional regulation of gene expression related to the control of mRNA stability and discuss their relevance in regulating cytokine expression linked to the inflammatory processes in kidney. Despite the fact that not many such examples in human kidney diseases have been uncovered with great mechanistic details, studies in experimental models suggest that the mRNA stability control is more than meets the eye. Therapeutic potentials aiming at regulating cytokine expression via posttranscriptional modification of mRNA half-life are thus discussed.


KEY WORDS: Nephritis - RNA - Cytokines

inizio pagina