title: [Molecular mechanisms involved in kidney ischemia-reperfusion].
abstract: Acute renal failure (ARF) is still associated with high mortality. It is the consequence of a set of phenomena leading to a low glomerular filtration rate resulting, at least partly, from a misregulation of renal blood flow resulting itself from injuries at the epithelial and endothelial level. The outer medulla seems to be the region of the kidney the most affected by ischemia. Investigation at the histological level reveals a partial destruction of the renal epithelium generated by necrosis and/or apoptosis, loss of cell polarity, cell desquamation into the lumen and endothelial cell swelling. The recent advances in the comprehension of this pathology underline the major role of inflammation, which is probably responsible for the worsening and the persistence of ARF. Studies at the molecular level have pinpointed the implication of many signalling pathways such as apoptosis, G-protein signalling, various receptor and kinase activation. The characterisation of the molecular events involved in ARF should help in our approaches to prevent and treat ARF. The understanding of the adaptation mechanisms to ischemic stress (conditioning) is probably one of the most promising research area of this field in terms of medical applications.
authors.affiliation: Groupe rein, Institut de génomique fonctionnelle, CNRS UMR5203, Inserm U661-UM1-UM2, 141, rue de la Cardonille, 34396 Montpellier cedex 05, France.
authors.forename: Stephan
authors.initials: S
authors.lastname: Soullier
authors.forename: Nathalie
authors.initials: N
authors.lastname: Gayrard
authors.forename: Catherine
authors.initials: C
authors.lastname: Méjean
authors.forename: Ilan
authors.initials: I
authors.lastname: Swarcz
authors.forename: Georges
authors.initials: G
authors.lastname: Mourad
authors.forename: Angel
authors.initials: A
authors.lastname: Argilés
mesh_terms: D000818:Animals; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D019194:Ischemic Preconditioning; D007668:Kidney / Q000098:blood supply* / Q000502:physiology*; D012038:Regeneration; D015424:Reperfusion