title: [Strategies to reverse fibrotic lesions of the kidney].
abstract: The deterioration of renal function in chronic kidney disease is related to the progression of renal fibrosis, which was long considered unavoidable. Today, the reversibility of renal fibrotic lesions is a reality, although still clinically rare. Because angiotensin II is highly profibrotic, blocking its action effectively protects the kidney, as numerous clinical trials have shown. The development of interstitial fibrosis is secondary to the epithelial-to-mesenchymal transition induced by transforming growth factor (TGF)-beta. Bone morphogenic protein-7 (BMP-7) and hepatocyte growth factor (HGF) induce the reverse transition and thus open up perspectives for treatment. Degradation of the extracellular matrix by matrix metalloproteinases or other enzymes is another therapeutic pathway. Renal regeneration may be promoted by modulation of hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF).
authors.affiliation: Service néphrologie et dialyses, Hôpital Tenon, AP-HP, Paris. jean-jacques.boffa@tnn.aphp.fr
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Boffa
authors.forename: Pierre
authors.initials: P
authors.lastname: Ronco
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D019485:Bone Morphogenetic Proteins / Q000502:physiology; D018450:Disease Progression; D004847:Epithelial Cells / Q000166:cytology; D005109:Extracellular Matrix / Q000378:metabolism; D005355:Fibrosis / Q000378:metabolism / Q000628:therapy*; D017228:Hepatocyte Growth Factor / Q000502:physiology; D006801:Humans; D007668:Kidney / Q000473:pathology* / Q000502:physiology; D008648:Mesoderm / Q000166:cytology; D012038:Regeneration; D016212:Transforming Growth Factor beta / Q000378:metabolism
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D019485:Bone Morphogenetic Proteins; D016212:Transforming Growth Factor beta; D017228:Hepatocyte Growth Factor