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- W2586440809 abstract "In the past years, optimization of immunosuppressive protocols considerably reduced the incidence of acute rejection after kidney transplantation. In contrast, very little progress has been achieved in the field of long-term transplant function and survival. Chronic allograft dysfunction still represents a major cause of graft loss and the underlying multi-factorial reasons involving both immunological and non-immunological aspects remain poorly understood. In the clinical setting prevention of ischemia-reperfusion injury as a non-immunological factor is achieved by cold preservation and particular perfusion solutions, whereas effective renoprotective treatment options after transplantation are still lacking. As prolonged ischemia not only leads to early tissue damage with reduced graft function, but also exhibits deteriorating long-term effects on the transplant kidney by increasing immunogenicity and predisposition to fibrosis, we aimed to identify new treatment strategies to counter or even reverse this clinical disease pattern. The precise part of different renal structures and components in kidney dysfunction and the effects of endothelial progenitor cell therapy were analyzed in a murine model of ischemia-reperfusion injury using 99m Tc-MAG3 scintigraphy, assessment of laser Doppler perfusion, examination of kidney-relevant parameters in blood and urine, as well as histological analysis. Without treatment, ischemia-reperfusion injury exhibited a substantial reduction of renal function with no evidence for regeneration, considerable tissue damage, and marked impairment of organ perfusion. Progenitor cell therapy potently enhanced vascular regeneration with increased perfusion and excellent tissue vitality, but had only limited beneficial effect on functional impairment. Histological analysis conclusively confirmed functional findings. Here, we show that cell-based therapy using endothelial progenitor c ells represents ap romising strategy to suspend the deteriorating cascade of events following ischemia-reperfusion injury. This novel treatment modality may aid to prolong allograft function and survival after kidney transplantation. Einleitung Durch die Verbesserung der immunsuppressiven Behandlungsmoglichkeiten konnte die akute Abstosungsrate nach Nierentransplantation in den vergangenen Jahren erheblich verringert werden. Dagegen sind hinsichtlich des Langzeit-Transplantatuberlebens nur geringe Fortschritte zu verzeichnen. Die chronische Transplantatdysfunktion stellt noch immer einen masgeblichen Grund fur den Verlust eines Transplantats dar. Die zugrundeliegenden multifaktoriellen immunologischen und nicht-immunologischen Ursachen sind in weiten Teilen noch unverstanden. Im klinischen Alltag verhindern kalte Ischamie und speziellle Aufbewahrungslosungen Schaden beim Nierentransplantat wahrend des Transports zum Empfanger. Dagegen stehen nach der Transplantation keine effektiven renoprotektiven Therapiemasnahmen zur Verfugung. Da lange Ischamiezeiten nicht nur kurzfristige Funktionseinschrankungen und Gewebeschaden hervorrufen, sondern auch erhebliche chronische" @default.
- W2586440809 created "2017-02-17" @default.
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- W2586440809 date "2009-01-01" @default.
- W2586440809 modified "2023-09-24" @default.
- W2586440809 title "Zelltherapie mit endothelialen Progenitorzellen bewahrt die Niere vor Ischämie-Reperfusionsschaden Cell-based therapy using endothelial progenitor cells rescues kidney from ischemia-reperfusion injury" @default.
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