Erythropoietin protects against ischaemic acute renal injury

Vesey, David A.; Cheung, Catherine; Pat, Betty; Endre, Zoltán H.; Gobé, Glenda C.; Johnson, David W.

doi:10.1093/ndt/gfg547

Cited by 259 publications

(219 citation statements)

References 31 publications

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“…While erythropoietin receptors Group 1; sham, group 2: GM treated for 10 days (positive control), group 3: GM treated for 10 days following by Eprex treated for 10 days, group 4; GM plus Eprex treated for 10 days. Ns: non-significant, ∆: concentration difference (after-before) are expressed on renal tubular epithelial cells (15,31), it is possible that the systemic administration of erythropoietin may also provide protection against acute renal damage (15, 31). Erythropoietin has also been found to ameliorate toxic renal injury caused by Cisplatin (31,32).…”

Section: Discussionmentioning

confidence: 99%

“…Ns: non-significant, ∆: concentration difference (after-before) are expressed on renal tubular epithelial cells (15,31), it is possible that the systemic administration of erythropoietin may also provide protection against acute renal damage (15, 31). Erythropoietin has also been found to ameliorate toxic renal injury caused by Cisplatin (31,32). Similarly, its renoprotective effect in ischemia-reperfusion renal injury, as the most common cause of ARF in the community was also reported (15,31).…”

Section: Discussionmentioning

confidence: 99%

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Erythropoietin ameliorates genetamicin-induced renal toxicity: A biochemical and histopathological study

et al. 2012

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Background:Investigations have attempted to modify the outcome of tubular injury by either ameliorating renal tubular damage or promoting tubular regeneration in the case of acute tubular necrosis. Objectives: We investigated the protective effect of Eprex an erythropoietin analogue on tubular injury induced by gentamicin (GM). Materials and Methods: Forty male Wistar rats were randomly divided into four groups. In group 1,rats were served as a sham group. In group 2, rats were injected intraperitoneally with 100 mg/kg of GM for 10 consecutive days (positive control group) and then were sacrificed. In group 3, rats received GM for 10 days then Eprex 100U/kg was injected intraperitoneally for the next 10 days and then they were sacrificed at the day 20th. In group 4 rats were injected a combination of GM (80 mg/kg) and Eprex 100U/kg intraperitoneally for 10 days and then were sacrificed. Results: The results indicated that, Eprex prevented the increase in serum creatinine (Cr) and blood urea nitrogen (BUN). The effect of Eprex on damage score, showed that co-administration of GM and Eprex (group 3 and 4) reduced the kidney tissue damage compared to positive control group (P<0.05). This result indicat that Eprex potentially can reduce or prevent the kidney tissue damage. Conclusions: Ameliorative effect of Eprex when the drug was given in combination with GM and also when the drug was applied after GM-induced tubular damage, revealed the renoprotective potency of Eprex. Eprex is a promising drug to prevent or attenuate tubular damage induced by GM or other nephrotoxic agents which act through the same mechanisms as gentamicin.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Erythropoietin ameliorates genetamicin-induced renal toxicity: A biochemical and histopathological study

et al. 2012

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“…72 The kidney is protected by EPO in the setting of both ischemic and toxic injuries. [73][74][75] In ischemic injury with reperfusion, EPO prevents apoptosis of tubular epithelial cells as well as mediates intense mitotic activity of the surviving population of proximal tubular epithelial cells. 73 The skin has also been shown to be protected by EPO in rodent flap models.…”

Section: Epo Signaling In Nervous System Cellsmentioning

confidence: 99%

“…[73][74][75] In ischemic injury with reperfusion, EPO prevents apoptosis of tubular epithelial cells as well as mediates intense mitotic activity of the surviving population of proximal tubular epithelial cells. 73 The skin has also been shown to be protected by EPO in rodent flap models. 76,77 In these studies, the tissue-protective effects appear to depend strongly on the dose and treatment duration, suggesting that tissues may vary in their responses to EPO.…”

Section: Epo Signaling In Nervous System Cellsmentioning

confidence: 99%

Erythropoietin as an antiapoptotic, tissue-protective cytokine

Ghezzi

Brines²

2004

Cell Death Differ

306

238

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Erythropoietin (EPO) increases the number of circulating erythrocytes primarily by preventing apoptosis of erythroid progenitors. In addition to this proerythroid action, results of recent studies show that systemically administered EPO is protective in vivo, in several animal models of neuronal injury. In vitro, EPO prevents neuronal apoptosis induced by a variety of stimuli. This review summarizes the neuroprotective actions of EPO and discusses the underlying mechanisms in terms of signal transduction pathways involved. The understanding of these mechanisms will help differentiate the neuroprotective actions of EPO from its role in the bone marrow.

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“…The role of HIF-1 on the survival of epithelial cells is obviously multifactorial, 47 but overall it promotes cell survival by mediating cellular adaptation to hypoxia. Both EPO and VEGF, which are induced by HIF, have been shown to protect renal tubular cells from apoptosis, 48,49 which may have contributed to the antiapoptotic effect of HIF demonstrated in the remnant kidney.…”

Section: Hif-mediated Angiogenesis In the Kidneymentioning

confidence: 99%

Cobalt promotes angiogenesis via hypoxia-inducible factor and protects tubulointerstitium in the remnant kidney model

Tanaka

Kojima

Ohse

et al. 2005

Laboratory Investigation

219

141

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Tubulointerstitial hypoxia has been implicated in a number of progressive renal diseases, and several lines of evidence indicate that the administration of angiogenic growth factors ameliorates tubulointerstitial injury. We hypothesized that induction of hypoxia-inducible factors (HIF) mediates renoprotection by their angiogenic properties. At 5-9 weeks after subtotal nephrectomy, cobalt was administered to rats to activate HIF. Histological evaluation demonstrated that the tubulointerstitial injury was significantly ameliorated in animals that received cobalt (score: 2.5170.12 (cobalt) vs 3.2170.24 (vehicle), Po0.05). Furthermore, animals receiving cobalt had fewer vimentin-and TdT-mediated dUTP nick-end labeling (TUNEL)-positive tubular cells. The renoprotective effect of cobalt was associated with the preservation of peritubular capillary networks (rarefaction index: 13.770.4 (cobalt) vs 18.670.9 (vehicle), Po0.01). This improvement in capillary networks was accompanied by an increased number of proliferating (PCNA-positive) glomerular and peritubular endothelial cells. The angiogenesis produced by this method was not accompanied by an increase in vascular permeability. Furthermore, in vitro experiments clarified that HIF-1 in tubular epithelial cells promotes proliferation of endothelial cells and that HIF-2 overexpressed in renal endothelial cells mediates migration and network formation. Collectively, these findings demonstrate a renoprotective role of HIF through angiogenesis and provide a rationale for therapeutic approaches to target HIF for activation.

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Erythropoietin protects against ischaemic acute renal injury

Abstract: The results suggest that, in addition to its well-known erythropoietic effects, EPO inhibits apoptotic cell death, enhances tubular epithelial regeneration and promotes renal functional recovery in hypoxic or ischaemic acute renal injury.

Cited by 259 publications

References 31 publications

Erythropoietin ameliorates genetamicin-induced renal toxicity: A biochemical and histopathological study

Erythropoietin ameliorates genetamicin-induced renal toxicity: A biochemical and histopathological study

Erythropoietin as an antiapoptotic, tissue-protective cytokine

Cobalt promotes angiogenesis via hypoxia-inducible factor and protects tubulointerstitium in the remnant kidney model

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