ArticleCells2022
Chronic Hyperglycemia Compromises Mitochondrial Function in Corneal Epithelial Cells: Implications for the Diabetic Cornea.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- High Glucose Induces Biomolecular Dysregulation in Primary Human Corneal Epithelial Cells: Potential Biomarkers of Hyperglycemia-Driven Corneal Impairment.International journal of molecular sciences · 2026Article
- LDN-27219 Modulates High-Glucose-Induced Endothelial Bioenergetic Remodeling and MitoSOX Red Fluorescence.Life (Basel, Switzerland) · 2026Article
- ELF3 promotes hyperglycemia-induced corneal epithelial senescence and IL-2 attenuates ELF3-associated signaling.Frontiers in molecular biosciences · 2026Article
- Article
- Effects of Benzalkonium Chloride, a Preservative in Topical Drugs, on the Barrier Function of Human Corneal Epithelial Cells.Translational vision science & technology · 2025Article
- Tear proteomics reveals expressed proteins and potential pathways associated with diabetic keratopathy.Eye (London, England) · 2025Article
- DJ-1 Promotes Diabetic Corneal Epithelial Wound Healing by Attenuating Hyperglycemia-Induced Oxidative Stress Through Inhibiting PTEN.Investigative ophthalmology & visual science · 2025Article
- Mitochondrial aldehyde dehydrogenase restores the migratory capacity inhibited by high glucose-induced hyperosmolality.Scientific reports · 2025Article
- IL-1β-Mediated Immunometabolic Adaptation in Corneal Epithelial Cells.Journal of inflammation research · 2025Article
- Mitochondria Transplantation Promotes Corneal Epithelial Wound Healing.Investigative ophthalmology & visual science · 2024Article
- Diabetic Ocular Surface Has Defects in Oxygen Uptake Revealed by Optic Fiber Microsensor.Investigative ophthalmology & visual science · 2024Article
- Peroxisome proliferator-activated receptor-α (PPARα) regulates wound healing and mitochondrial metabolism in the cornea.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The roles of autophagy and mitophagy in corneal pathology: current knowledge and future perspectives.Frontiers in medicine · 2023Review
- Irisin Ameliorates Renal Tubulointerstitial Fibrosis by Regulating the Smad4/β-Catenin Pathway in Diabetic Mice.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction is a major pathophysiological event leading to the onset of diabetic complications. This study investigated the temporal effects of hyperglycemia on mitochondrial metabolism in corneal epithelial cells. To accomplish this, human telomerase-immortalized corneal epithelial cells were cultured in a defined growth medium containing 6 mM glucose. To simulate hyperglycemia, cells were cultured in a medium containing 25 mM D-glucose, and control cells were cultured in mannitol. Using metabolic flux analysis, there was a hyperosmolar-mediated increase in mitochondrial respiration after 24 h. By day 5, there was a decrease in spare respiratory capacity in cells subject to high glucose that remained suppressed throughout the 14-day period. Although respiration remained high through day 9, glycolysis was decreased. Mitochondrial respiration was decreased by day 14. This was accompanied by the restoration of glycolysis to normoglycemic levels. These changes paralleled a decrease in mitochondrial polarization and cell cycle arrest. Together, these data show that chronic but not acute hyperglycemic stress leads to mitochondrial dysfunction. Moreover, the hyperglycemia-induced loss of spare respiratory capacity reduces the ability of corneal epithelial cells to respond to subsequent stress. Compromised mitochondrial function represents a previously unexplored mechanism that likely contributes to corneal complications in diabetes.
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What Socratic holds
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 Socratic graph.