title: [The role of endothelial progenitor cells in renal disease].
abstract: Recent evidence suggests that injury to the renal vasculature may play an important role in the pathogenesis of both chronic and acute ischemic kidney injury. Early alterations in peritubular capillary blood flow during reperfusion have been documented and associated with loss of normal endothelial cell function. In addition, ischemia induces alterations in endothelial cells that may promote inflammation and procoagulant activity, thus contributing to vascular congestion. Reduction of the microvasculature density increases hypoxia-mediated fibrosis and alters proper hemodynamics, which may lead to hypertension. This may play a critical role in the progression of chronic kidney disease following initial recovery from ischemia/reperfusion-induced acute kidney injury. The turnover and replacement of endothelial cells is therefore an important mechanism in the maintenance of vascular integrity also in the kidney. It is becoming clear that impaired vascular repair mechanisms as a result of a reduced number and/or impaired function of endothelial progenitor cells may contribute to renal disease. Moreover, investigators have begun to identify potential mechanisms responsible for the loss of function of endothelial progenitors in renal disease. In allografts, persistent injury results in excessive turnover of graft vascular endothelial cells. Moreover, chronic damage elicits a response that is associated with the recruitment of both leukocytes and endothelial progenitors, facilitating an overlapping process of inflammation and angiogenesis. In conclusion, angiogenesis and endothelial cell turnover play a pivotal role in renal disease and allograft rejection. Manipulation of these processes might have important implications for the development of novel therapeutic strategies in the near future.
authors.affiliation: Centro Interdipartimentale di Nefrologia Cellulare e Molecolare, Centro di Eccellenza per il Trasferimento, la Ricerca e l'Alta Formazione DENOthe, Universita' degli Studi, Viale Pieraccini 6, Florence, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Lazzeri
authors.forename: M L
authors.initials: ML
authors.lastname: Angelotti
authors.forename: L
authors.initials: L
authors.lastname: Ballerini
authors.forename: F
authors.initials: F
authors.lastname: Becherucci
authors.forename: B
authors.initials: B
authors.lastname: Mazzinghi
authors.forename: E
authors.initials: E
authors.lastname: Parente
authors.forename: E
authors.initials: E
authors.lastname: Ronconi
authors.forename: C
authors.initials: C
authors.lastname: Sagrinati
authors.forename: P
authors.initials: P
authors.lastname: Romagnani
authors.forename: L
authors.initials: L
authors.lastname: Lasagni
mesh_terms: D002908:Chronic Disease; D018450:Disease Progression; D042783:Endothelial Cells / Q000502:physiology*; D006801:Humans; D007511:Ischemia / Q000209:etiology; D007668:Kidney / Q000098:blood supply; D007674:Kidney Diseases / Q000209:etiology* / Q000601:surgery; D016030:Kidney Transplantation; D013234:Stem Cells / Q000502:physiology*