ReviewBioMed research international2014
Hypoxia in diabetic kidneys.
Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 103 citations in OpenAlex.
- The endothelium response to kidney injury.Nature reviews. Nephrology · 2026Review
- Cardiovascular Protection in Coronary Artery Disease: Mechanistic and Clinical Insights into SGLT2 Inhibitors and GLP-1 Receptor Agonists.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Cell-type specific effects of the long non-coding RNA HIF1A-AS3 on HIF1A expression in kidney cells.Scientific reports · 2025Article
- Metformin as a Modulator of Autophagy and Hypoxia Responses in the Enhancement of Wound Healing in Diabetic Rats.Inflammation · 2025Article
- High glucose/ChREBP-induced Hif-1α transcriptional activation in CD4Diabetologia · 2025Article
- Metformin Protects Human Induced Pluripotent Stem Cell (hiPSC)-Derived Neurons from Oxidative Damage Through Antioxidant Mechanisms.Neurotoxicity research · 2025Article
- From Microcirculation to Aging-Related Diseases: A Focus on Endothelial SIRT1.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Renoprotective effect of a novel combination of 6-gingerol and metformin in high-fat diet/streptozotocin-induced diabetic nephropathy in rats via targeting miRNA-146a, miRNA-223, TLR4/TRAF6/NLRP3 inflammasome pathway and HIF-1α.Biological research · 2024Article
- The Renoprotective Mechanisms of Sodium-Glucose Cotransporter-2 Inhibitors (SGLT2i)-A Narrative Review.International journal of molecular sciences · 2024Review
- Canagliflozin ameliorates high glucose-induced apoptosis in NRK-52E cells via inhibiting oxidative stress and activating AMPK/mTOR-mediated autophagy.Molecular biology reports · 2023Article
- The therapeutic prospect of zinc oxide nanoparticles in experimentally induced diabetic nephropathy.Tissue barriers · 2023Article
- Targeting inflammation for the treatment of Diabetic Kidney Disease: a five-compartment mechanistic model.BMC nephrology · 2022Review
- Telomere Lengths and Serum Proteasome Concentrations in Patients with Type 1 Diabetes and Different Severities of Diabetic Retinopathy in Latvia and Lithuania.Journal of clinical medicine · 2022Article
- Biochemical mechanism underlying the pathogenesis of diabetic retinopathy and other diabetic complications in humans: the methanol-formaldehyde-formic acid hypothesis.Acta biochimica et biophysica Sinica · 2022Article
- An Overview of the Cardiorenal Protective Mechanisms of SGLT2 Inhibitors.International journal of molecular sciences · 2022Review
- Colorimetric and Electrochemical Screening for Early Detection of Diabetes Mellitus and Diabetic Retinopathy-Application of Sensor Arrays and Machine Learning.Sensors (Basel, Switzerland) · 2022Review
- Mechanistic Pathogenesis of Endothelial Dysfunction in Diabetic Nephropathy and Retinopathy.Frontiers in endocrinology · 2022Review
- Review
- Transcription Factor ChREBP Mediates High Glucose-Evoked Increase in HIF-1α Content in Epithelial Cells of Renal Proximal Tubules.International journal of molecular sciences · 2021Article
- Cardiorenal Syndrome: Emerging Role of Medical Imaging for Clinical Diagnosis and Management.Journal of personalized medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is now a leading cause of end-stage renal disease. In addition, DN accounts for the increased mortality in type 1 and type 2 diabetes, and then patients without DN achieve long-term survival compatible with general population. Hypoxia represents an early event in the development and progression of DN, and hypoxia-inducible factor- (HIF-) 1 mediates the metabolic responses to renal hypoxia. Diabetes induces the "fraternal twins" of hypoxia, that is, pseudohypoxia and hypoxia. The kidneys are susceptible to hyperoxia because they accept 20% of the cardiac output. Therefore, the kidneys have specific vasculature to avoid hyperoxia, that is, AV oxygen shunting. The NAD-dependent histone deacetylases (HDACs) sirtuins are seven mammalian proteins, SIRTs 1-7, which are known to modulate longevity and metabolism. Recent studies demonstrated that some isoforms of sirtuins inhibit the activation of HIF by deacetylation or noncatalyzing effects. The kidneys, which have a vascular system that protects them against hyperoxia, unfortunately experience extraordinary hypernutrition today. Then, an unexpected overload of glucose augments the oxygen consumption, which ironically results in hypoxia. This review highlights the primary role of HIF in diabetic kidneys for the metabolic adaptation to diabetes-induced hypoxia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.