ReviewFrontiers in medicine2021
Tubular Cell Glucose Metabolism Shift During Acute and Chronic Injuries.
Review in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
36 citing papers in PubMed, 66 citations in OpenAlex.
- Lactate in acute kidney injury: pathobiology, risk stratification, and clinical interpretation.Renal failure · 2026Review
- Epigenetically silencing gluconeogenic enzyme PCK1 by EZH2 promotes renal tubulointerstitial fibrosis.Molecular biomedicine · 2026Article
- Renal glucose metabolic enzyme expression during AKI-to-CKD transition.International urology and nephrology · 2026Article
- Ablation of the renal tubular gluconeogenic enzyme PCK1 drives AKI-to-CKD transition by negatively regulating the TGF-β/Smad3 signaling pathway.Cellular and molecular life sciences : CMLS · 2026Article
- From AKI to CKD mechanisms of maladaptive repair and disease progression.International urology and nephrology · 2026Review
- Sexual dimorphism shapes renal metabolic adaptation to a ketogenic diet.Cell reports · 2026Article
- Chronic NHScientific reports · 2026Article
- KiScience · 2025Article
- The new insights of lactate in various kidney diseases.Expert reviews in molecular medicine · 2025Review
- Non-Diabetic Hypoglycemia: Evaluation and Management in Adults.Journal of clinical medicine · 2025Review
- Glycolytic control proteins in urinary extracellular vesicles are elevated during kidney transplant T cell-mediated rejection.BMC nephrology · 2025Observational
- Autophagy Related 5 Promotes Mitochondrial Fission and Inflammation via HSP90-HIF-1α-Mediated Glycolysis in Kidney Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Modulation of the thiol redox proteome by sugarcane ash-derived silica nanoparticles: insights into chronic kidney disease of unknown etiology.Particle and fibre toxicology · 2025Article
- A Newly Identified Protective Role of C5a Receptor 1 in Kidney Tubules against Toxin-Induced Acute Kidney Injury.The American journal of pathology · 2025Article
- Tanshinone I improves renal fibrosis by promoting gluconeogenesis through upregulation of peroxisome proliferator-activated receptor-γ coactivator 1α.Renal failure · 2024Article
- Identification of Spatial Specific Lipid Metabolic Signatures in Long-Standing Diabetic Kidney Disease.Metabolites · 2024Article
- Interactions of SARS-CoV-2 with Human Target Cells-A Metabolic View.International journal of molecular sciences · 2024Review
- Review
- Forkhead Box Protein K1 Promotes Chronic Kidney Disease by Driving Glycolysis in Tubular Epithelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The e-liquid flavoring cinnamaldehyde induces cellular stress responses in human proximal tubule (HK-2) kidney cells.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute and chronic kidney disease are responsible for large healthcare costs worldwide. During injury, kidney metabolism undergoes profound modifications in order to adapt to oxygen and nutrient shortage. Several studies highlighted recently the importance of these metabolic adaptations in acute as well as in chronic phases of renal disease, with a potential deleterious effect on fibrosis progression. Until recently, glucose metabolism in the kidney has been poorly studied, even though the kidney has the capacity to use and produce glucose, depending on the segment of the nephron. During physiology, renal proximal tubular cells use the beta-oxidation of fatty acid to generate large amounts of energy, and can also produce glucose through gluconeogenesis. In acute kidney injury, proximal tubular cells metabolism undergo a metabolic shift, shifting away from beta-oxidation of fatty acids and gluconeogenesis toward glycolysis. In chronic kidney disease, the loss of fatty acid oxidation is also well-described, and data about glucose metabolism are emerging. We here review the modifications of proximal tubular cells glucose metabolism during acute and chronic kidney disease and their potential consequences, as well as the potential therapeutic implications.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.