ArticlePloS one2016
Hyperglycemia Induces Cellular Hypoxia through Production of Mitochondrial ROS Followed by Suppression of Aquaporin-1.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.
- Pooled it
- Trial
- The anti-obesity and hepatoprotective effects of bacterial cyclodipeptides in a rat obesity model involve aquaporins, inflammatory factors, and GAB1 modulation.Journal of physiology and biochemistry · 2026Article
- Article
- Imaging Hypoxia in the Diabetic Retina: A Potential Early-Detection Imaging Biomarker Before Detectable Retinopathy in Diabetes.Diabetes · 2026Article
- Unravelling the pathophysiology of diabetic foot ulcer: insights into a complex wound healing process.Frontiers in clinical diabetes and healthcare · 2026Review
- Imaging of the retinal hypoxia: A journey from oxygen microelectrode to the first hypoxia imaging in the living retina.Progress in retinal and eye research · 2025Review
- "Hyperglycemic Memory": Observational Evidence to Experimental Inference.Current diabetes reviews · 2025Review
- Plant-inspired visible-light-driven bioenergetic hydrogels for chronic wound healing.Bioactive materials · 2024Article
- Aquaporin 1 confers apoptosis resistance in pulmonary arterial smooth muscle cells from the SU5416 hypoxia rat model.Physiological reports · 2024Article
- SARS-CoV-2 Infection Positively Correlates with Hyperglycemia and Inflammatory Markers in COVID-19 Patients: A Clinical Research Study.Diseases (Basel, Switzerland) · 2024Article
- Role of Hsa_circ_0000880 in the Regulation of High Glucose-Induced Apoptosis of Retinal Microvascular Endothelial Cells.Translational vision science & technology · 2024Article
- Hypoxia suppresses glucose-induced increases in collective cell migration in vascular endothelial cell monolayers.Scientific reports · 2024Article
- Important functions and molecular mechanisms of aquaporins family on respiratory diseases: potential translational values.Journal of Cancer · 2024Review
- Staining Hypoxic Areas of Frozen and FFPE Tissue Sections with Hypoxyprobe™.Methods in molecular biology (Clifton, N.J.) · 2024Article
- The role of heat shock proteins in the pathogenesis of heart failure (Review).International journal of molecular medicine · 2023Review
- Article
- Article
- Recent advances in molecular biology of metabolic syndrome pathophysiology: endothelial dysfunction as a potential therapeutic target.Journal of diabetes and metabolic disorders · 2022Review
- MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously proposed that hyperglycemia-induced mitochondrial reactive oxygen species (mtROS) generation is a key event in the development of diabetic complications. Interestingly, some common aspects exist between hyperglycemia and hypoxia-induced phenomena. Thus, hyperglycemia may induce cellular hypoxia, and this phenomenon may also be involved in the pathogenesis of diabetic complications. In endothelial cells (ECs), cellular hypoxia increased after incubation with high glucose (HG). A similar phenomenon was observed in glomeruli of diabetic mice. HG-induced cellular hypoxia was suppressed by mitochondria blockades or manganese superoxide dismutase (MnSOD) overexpression, which is a specific SOD for mtROS. Overexpression of MnSOD also increased the expression of aquaporin-1 (AQP1), a water and oxygen channel. AQP1 overexpression in ECs suppressed hyperglycemia-induced cellular hypoxia, endothelin-1 and fibronectin overproduction, and apoptosis. Therefore, hyperglycemia-induced cellular hypoxia and mtROS generation may promote hyperglycemic damage in a coordinated manner.
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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.