Expression of Transforming Growth Factor-β1 and Hypoxia-Inducible Factor-1α in Renal Transplantation

Lee, S.; Kim, D.J.; Park, M.G.; Park, S.K.; Kim, J.S.; Hyun, Seungjoon; Oh, Ji Eun; Nam, Eun Sook; Joo, Sun Hyung

doi:10.1016/j.transproceed.2008.06.054

Cited by 3 publications

(2 citation statements)

References 3 publications

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“…The effect of the interaction between HIF and TGF-β pathway on the recipients’ immune status, and how this may affect long-term allograft function is not known. However, profiling of biopsy tissues from chronic allograft nephropathy (CAN) patients showed significantly higher expression of both HIF-1α and TGF-β1 compared to the group without CAN [ 33 ].…”

Section: Role Of Hypoxia and Hypoxia-inducible Factor (Hif)mentioning

confidence: 99%

Ischaemia reperfusion injury: mechanisms of progression to chronic graft dysfunction

Situmorang

Sheerin

2018

Pediatr Nephrol

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The increasing use of extended criteria organs to meet the demand for kidney transplantation raises an important question of how the severity of early ischaemic injury influences long-term outcomes. Significant acute ischaemic kidney injury is associated with delayed graft function, increased immune-associated events and, ultimately, earlier deterioration of graft function. A comprehensive understanding of immediate molecular events that ensue post-ischaemia and their potential long-term consequences are key to the discovery of novel therapeutic targets. Acute ischaemic injury primarily affects tubular structure and function. Depending on the severity and persistence of the insult, this may resolve completely, leading to restoration of normal function, or be sustained, resulting in persistent renal impairment and progressive functional loss. Long-term effects of acute renal ischaemia are mediated by several mechanisms including hypoxia, HIF-1 activation, endothelial dysfunction leading to vascular rarefaction, sustained pro-inflammatory stimuli involving innate and adaptive immune responses, failure of tubular cells to recover and epigenetic changes. This review describes the biological relevance and interaction of these mechanisms based on currently available evidence.

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Section: Role Of Hypoxia and Hypoxia-inducible Factor (Hif)mentioning

confidence: 99%

Ischaemia reperfusion injury: mechanisms of progression to chronic graft dysfunction

Situmorang

Sheerin

2018

Pediatr Nephrol

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“…Regardless of the insult causing tissue injury following transplantation, the response to injury consists of both a proliferative response and an inflammatory response, culminating in extracellular matrix deposition. Transforming growth factor beta (TGF-β) has long been recognized as a mediator of loss of kidney function with IF/TA in both humans [54, 56–58] and rodents [59]. TGF-β is a multifunctional peptide that stimulates the synthesis of individual extracellular matrix components, and blocks matrix degradation by stimulating protease inhibitors such as plasminogen activator inhibitor-1 (PAI-1) [60].…”

Section: Differentially Expressed Genes In Chronic Allograft Nephropamentioning

confidence: 99%

Molecular pathways involved in loss of graft function in kidney transplant recipients

Mas¹,

Archer²,

Scian³

et al. 2010

Expert Review of Molecular Diagnostics

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Interstitial fibrosis (IF) and tubular atrophy (TA) are integral parts of chronic allograft dysfunction and represent in the new classification a separate entity with or without the identification of a specific etiology. Loss of kidney graft function with IF/TA is one of the causes of most kidney allograft losses. Despite progress in immunosuppression, chronic allograft dysfunction remains the main clinical challenge for improving long-term graft survival. The sustained damage to the allograft does not represent a single entity but the summated effects of tissue injury from several pathogenic insults, as well as the kidney's healing response, modified by alloimmunity and immunosuppression. A major challenge in the future of kidney transplantation includes the study of chronic allograft dysfunction pathogenesis to identify early markers of disease progression, as well as potential therapeutics pathways.

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Serum Levels of Interleukin (IL)-10, IL-17, Transforming Growth Factor (TGF)-β1, and Interferon-γ Cytokines and Expression Levels of IL-10 and TGF-β1 Genes in Renal Allograft Recipients After Donor Bone Marrow Cell Infusion

Mohammadnia

Solgi

Ranjbar

et al. 2011

Transplantation Proceedings

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Expression of Transforming Growth Factor-β1 and Hypoxia-Inducible Factor-1α in Renal Transplantation

Cited by 3 publications

References 3 publications

Ischaemia reperfusion injury: mechanisms of progression to chronic graft dysfunction

Ischaemia reperfusion injury: mechanisms of progression to chronic graft dysfunction

Molecular pathways involved in loss of graft function in kidney transplant recipients

Serum Levels of Interleukin (IL)-10, IL-17, Transforming Growth Factor (TGF)-β1, and Interferon-γ Cytokines and Expression Levels of IL-10 and TGF-β1 Genes in Renal Allograft Recipients After Donor Bone Marrow Cell Infusion

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