ReviewClinical and experimental nephrology2016
Expanding roles of the hypoxia-response network in chronic kidney disease.
Review in Clinical and experimental nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- The pathological mechanisms and potential therapeutic strategies for renal anemia.Frontiers in pharmacology · 2026Review
- Hypoxia-inducible factor-1α promotes tubulointerstitial fibrosis via the upregulation ofRenal failure · 2025Article
- Prolyl hydroxylase domain inhibitors prevent kidney crystal formation by suppressing inflammation.Urolithiasis · 2024Article
- Metabolic reprogramming and renal fibrosis: what role might Chinese medicine play?Chinese medicine · 2024Review
- 3D hypoxia-mimicking and anti-synechia hydrogel enabling promoted neovascularization for renal injury repair and regeneration.Materials today. Bio · 2023Article
- Effects of long-term tubular HIF-2α overexpression on progressive renal fibrosis in a chronic kidney disease model.BMB reports · 2023Article
- Non-Invasive Assessment of Vascular Circulation Based on Flow Mediated Skin Fluorescence (FMSF).Biology · 2023Review
- TRIM46 upregulates Wnt/β-catenin signaling by inhibiting Axin1 to mediate hypoxia-induced epithelial-mesenchymal transition in HK2 cells.Molecular and cellular biochemistry · 2022Article
- Role of abnormal energy metabolism in the progression of chronic kidney disease and drug intervention.Renal failure · 2022Article
- Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022Review
- Current strategies and progress for targeting the "undruggable" transcription factors.Acta pharmacologica Sinica · 2022Review
- Hypoxia-Inducible Factors and Diabetic Kidney Disease-How Deep Can We Go?International journal of molecular sciences · 2022Review
- Renal hypoxia-HIF-PHD-EPO signaling in transition metal nephrotoxicity: friend or foe?Archives of toxicology · 2022Review
- Therapeutic potential of topical administration of acriflavine against hypoxia-inducible factors for corneal fibrosis.Frontiers in pharmacology · 2022Article
- Renoprotective Role of Hypoxia-Inducible Factors and the Mechanism.Kidney diseases (Basel, Switzerland) · 2022Review
- Roxadustat Attenuates the Disruption of Epithelial Tight Junction in Caco2 Cells and a Rat Model of CKD Through MicroRNA-223.Frontiers in medicine · 2022Article
- Hypoxia-induced preadipocyte factor 1 expression in human lung fibroblasts through ERK/PEA3/c-Jun pathway.Molecular medicine (Cambridge, Mass.) · 2021Article
- Contribution of Oxidative Stress to HIF-1-Mediated Profibrotic Changes during the Kidney Damage.Oxidative medicine and cellular longevity · 2021Review
- Treatment for renal anemia and outcomes in non-dialysis patients with chronic kidney disease: the current status of regional medicine according to the Kyoto Fushimi Renal Anemia (KFRA) study.Clinical and experimental nephrology · 2019Observational
- Mechanisms of hypoxia signalling: new implications for nephrology.Nature reviews. Nephrology · 2019Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies over the last two decades have established tubulointerstitial hypoxia as a final common pathway leading to end-stage kidney disease (ESKD). Chronic kidney disease (CKD) is frequently associated with various degrees of hypoxic injury in distinct tubular segments, depending on the etiology and pathological stages, which constitutes an intricate link among inflammation, oxidative stress and fibrosis. Resident cells in the kidney are equipped with mechanisms through which they cope with hypoxia. Here, transcription of genes by hypoxia-inducible factors (HIFs) plays a central role. In the ischemic kidney, HIF-1 is expressed in tubular and glomerular epithelial cells and in papillary interstitial cells, whereas HIF-2 is expressed in endothelial cells and interstitial fibroblasts. There is ample evidence that HIF protects the kidney from acute ischemic damage. In CKD, studies suggest that the function of HIF may be suppressed because of factors, such as oxidative stress and uremia, which may underlie the pathogenesis of both CKD and co-existing problems, such as renal anemia. Based on these observations, efforts are in progress to test whether restoration and activation of HIF might protect the kidney from CKD. Initial studies using non-specific or supraphysiological HIF activation suggested that the role of HIF may be multifactorial and depend on pathological context. On the other hand, specific HIF stabilizers, such as prolyl hydroxylase (PHD) inhibitors, are being developed for the treatment of renal anemia. Application of these compounds in experimental CKD may override those previous findings and provide deeper insight into the roles of hypoxia and oxygen-sensing pathways.
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