Advances in Understanding the Effects of Erythropoietin on Renal Fibrosis

Zhang, Yangyang; Zhu, Xiaoyu; Huang, Xiu; Wei, Xuejiao; Zhao, Dan; Jiang, Lili; Zhao, Xiyang; Du, Yujun

doi:10.3389/fmed.2020.00047

Cited by 14 publications

(4 citation statements)

References 85 publications

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“…Effective prevention and treatment of RF are of great significance for delaying the progression of kidney disease and reducing the occurrence of uremia. However, currently, there is no effective treatment for preventing and reversing RF [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Fer exacerbates renal fibrosis and can be targeted by miR-29c-3p

et al. 2021

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Aim Renal fibrosis (RF) is a common clinical condition leading to irreversible renal function loss. Tyrosine kinase proteins and microRNAs (miRs) are associated with pathogenesis and we aim to investigate the role of Fer and its partner miR(s) in RF. Method In silico reproduction of Mouse Kidney FibrOmics browser was performed to identify potential miR(s) and target gene(s). In vivo validation was performed in C57BL/6 mice with unilateral ureteral obstruction (UUO). In vitro validation was performed in rat kidney fibroblast NRK-49F cells. Mimics and inhibitors of miR-29c-3p were constructed. The target gene Fer was monitored by RT-PCR and western blotting. The levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α in serum and media were measured by ELISA. Results The Fer expression and protein level were gradually increased during 14 days of UUO modeling. miR-29c-3p expression was strongly correlated with that of Fer. In vivo validation showed increased expressions of fibrosis-associated genes and increased phospoho-Smad3 level in the UUO model. Fer-knockdown (KD) significantly decreased expressions of fibrosis-associated genes. Pharmaceutical inhibition of Fer showed similar effects to miR-29c-3p, and miR inhibition showed a significant decrease of excretion of inflammatory factors. Conclusion Dysregulation of miR-29c-3p and Fer plays a role in RF. Pharmaceutical or genetic inhibition of Fer may serve as the potential treatment for RF.

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Section: Introductionmentioning

confidence: 99%

Fer exacerbates renal fibrosis and can be targeted by miR-29c-3p

et al. 2021

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“…Besides, it was reported that the activation of the Pi3K/AKT pathway slows down tubular healing and increases renal fibrosis in IR injury-induced acute kidney injury. On the contrary, the treatment with EPO in the same model is associated with the prevention of programmed cellular death 51 . Our outcomes adhere to the aforementioned data in which the TAA-enhanced renal injury was associated with the activation of JAK2/PI3K/STAT5, another indirect pathway of STAT5 activation.…”

Section: Discussionmentioning

confidence: 96%

Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway

Elbaset,

Mohamed,

Gad

et al. 2023

Sci Rep

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The kidney flushes out toxic substances and metabolic waste products, and homeostasis is maintained owing to the kidney efforts. Unfortunately, kidney disease is one of the illnesses with a poor prognosis and a high death rate. The current investigation was set out to assess erythropoietin (EPO) potential therapeutic benefits against thioacetamide (TAA)-induced kidney injury in rats. EPO treatment improved kidney functions, ameliorated serum urea, creatinine, and malondialdehyde, increased renal levels of reduced glutathione, and slowed the rise of JAK2, STAT5, AMPK, and their phosphorylated forms induced by TAA. EPO treatment also greatly suppressed JAK2, Phosphatidylinositol 3-kinases, and The Protein Kinase R-like ER Kinase gene expressions and mitigated the histopathological alterations brought on by TAA toxicity. EPO antioxidant and anti-inflammatory properties protected TAA-damaged kidneys. EPO regulates AMPK, JAK2/STAT5, and pro-inflammatory mediator synthesis.

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“…34 Furthermore, it has been reported that EPO-H enhances the revival in acute kidney injury (AKI), and it improves proteinuria and blood biomarkers of kidney injury in CKD patients. 35 ESAs have essential protective effects on the kidneys and improve the prognosis in CKD patients. 36 These effects of ESAs were not supported by a study that reported EPO-receptor (EPO-R) protein was almost undetectable in renal cells, and there was no evidence of EPO-R expression and function in the studied group.…”

Section: Treatment ( Fig 1 )mentioning

confidence: 99%

Anemia in Chronic Kidney Disease Patients: An Update

Habas

Rayani

Habas

et al. 2022

Ibnosina Journal of Medicine and Biomedical Sciences

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Chronic kidney disease (CKD) is one of the most common disabling diseases globally. The main etiopathology of CKD is attributed to progressive renal fibrosis secondary to recurrent renal insults. Anemia is a known complication in CKD patients, associated with higher hospitalization rates and increased mortality risk. CKD-associated anemia (CKD-AA) is either due to true iron deficiency and/or functional iron deficiency anemia. There is new emerging evidence about the effects of erythropoiesis stimulating agents in the treatment of CKD-AA and their role in reversing and preventing kidney fibrosis in the early stages of CKD. This effect potentially provides new scopes in the prevention and treatment of CKD-AA and in decreasing the progression of CKD and the associated long-term complications. Epidemiology, pathophysiology, and treatments of CKD-AA will be discussed.

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Advances in Understanding the Effects of Erythropoietin on Renal Fibrosis

Cited by 14 publications

References 85 publications

Fer exacerbates renal fibrosis and can be targeted by miR-29c-3p

Fer exacerbates renal fibrosis and can be targeted by miR-29c-3p

Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway

Anemia in Chronic Kidney Disease Patients: An Update

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