title: [Reversal of renal fibrosis: lessons from experimental models].
abstract: New insights into the pathophysiological mechanisms of renal disease progression have been provided by recent experimental studies. It is now clear that angiotensin II is a key factor in the development of renal fibrosis, and that angiotensin II antagonists can slow the progression of renal disease in humans. However, other profibrotic agents, such as TGF beta, endothelin, and activated growth factor receptors have also been implicated. In vivo experimental studies have shown that renal fibrosis can be reversed. Based on the results of genetic and pharmacological antagonism of profibrotic agents in animals, this review describes potential future therapeutics that might limit the progression of human nephropathies, or even reverse them.
authors.affiliation: Unité INSERM 702, Hôpital Tenon, Paris, France.
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Dussaule
authors.forename: Christos
authors.initials: C
authors.lastname: Chatziantoniou
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D004195:Disease Models, Animal; D005355:Fibrosis; D006801:Humans; D007668:Kidney / Q000473:pathology*; D051436:Renal Insufficiency, Chronic / Q000188:drug therapy* / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000502:physiology
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers