ArticleAmerican journal of physiology. Renal physiology2024
Energy depletion by cell proliferation sensitizes the kidney epithelial cells to injury.
Article in American journal of physiology. Renal physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Mitigation of Ischemia/Reperfusion-Induced Acute Kidney Injury by Canagliflozin Is Associated with Altered Mitochondrial Dynamics and Reduced Proliferation in Swine.Biomolecules · 2026Article
- Alterations in Adenylate Nucleotide Metabolism and Associated Lipid Peroxidation and Protein Oxidative Damage in Rat Kidneys Under Combined Acetaminophen Toxicity and Protein Deficiency.Antioxidants (Basel, Switzerland) · 2026Article
- Review
- Longitudinal Multi-Organ Transcriptomic Atlas of Salt-Induced Hypertension.bioRxiv : the preprint server for biology · 2025Article
- Mechanisms of Cisplatin-Induced Acute Kidney Injury: The Role of NRF2 in Mitochondrial Dysfunction and Metabolic Reprogramming.Antioxidants (Basel, Switzerland) · 2025Article
- Biology of the proximal tubule in body homeostasis and kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- A Newly Identified Protective Role of C5a Receptor 1 in Kidney Tubules against Toxin-Induced Acute Kidney Injury.The American journal of pathology · 2025Article
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Acute kidney injury activates both proliferative and antiproliferative pathways, the consequences of which are not fully elucidated. If an initial proliferation of the renal epithelium is necessary for the successful repair, the persistence of proliferation markers is associated with the occurrence of chronic kidney disease. We hypothesized that proliferation in stress conditions impacts cell viability and renal outcomes. We found that proliferation is associated with cell death after various stresses in kidney cells. In vitro, the ATP/ADP ratio oscillates reproducibly throughout the cell cycle, and cell proliferation is associated with a decreased intracellular ATP/ADP ratio. In vivo, transcriptomic data from transplanted kidneys revealed that proliferation was strongly associated with a decrease in the expression of the mitochondria-encoded genes of the oxidative phosphorylation pathway, but not of the nucleus-encoded ones. These observations suggest that mitochondrial function is a limiting factor for energy production in proliferative kidney cells after injury. The association of increased proliferation and decreased mitochondrial function was indeed associated with poor renal outcomes. In summary, proliferation is an energy-demanding process impairing the cellular ability to cope with an injury, highlighting proliferative repair and metabolic recovery as indispensable and interdependent features for successful kidney repair.
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Registered trials
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