ReviewInternational journal of molecular sciences2018
Epithelial Cell Cycle Behaviour in the Injured Kidney.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 68 citations in OpenAlex.
- O-Glycosylation of E-Cadherin Induced by Endoplasmic Reticulum Stress Negatively Regulates Cell Polarity and Proliferation in Acute Kidney Injury.Journal of biochemical and molecular toxicology · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- What new renal biomarkers tell us about renal physiology: Collection: physiology applied to ICU.Annals of intensive care · 2026Review
- Minichromosome maintenance 4 plays a key role in protecting against acute kidney injury by regulating tubular epithelial cells survival and regeneration.Journal of advanced research · 2026Article
- MiR-503-5p mediates cell cycle arrest and fibrosis of peritoneal mesothelial cells with a high peritoneal solute transport status.BMC nephrology · 2025Article
- Advances in Nano-Immunomodulatory Systems for the Treatment of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- The inhibition of ZC3H13 attenuates G2/M arrest and apoptosis by alleviating NABP1 m6A modification in cisplatin-induced acute kidney injury.Cellular and molecular life sciences : CMLS · 2025Article
- Protective effect of Panax ginseng extract on cisplatin-induced AKI via downregulating cell death associated genes.Scientific reports · 2025Article
- The Kidney Precision Medicine Project and Single-Cell Biology of the Injured Proximal Tubule.The American journal of pathology · 2025Review
- Deficiency of purinergic P2Y2 receptor impairs the recovery after renal ischemia-reperfusion injury and accelerates renal fibrosis and tubular senescence in mice.Scientific reports · 2024Article
- Unlocking the mechanistic potential ofJournal of traditional and complementary medicine · 2024Review
- Renal tubular epithelial cells response to injury in acute kidney injury.EBioMedicine · 2024Review
- Cellular senescence of renal tubular epithelial cells in acute kidney injury.Cell death discovery · 2024Review
- The Therapeutic Potential of CDK4/6 Inhibitors, Novel Cancer Drugs, in Kidney Diseases.International journal of molecular sciences · 2023Review
- Incomplete Recovery from the Radiocontrast-Induced Dysregulated Cell Cycle, Adhesion, and Fibrogenesis in Renal Tubular Cells after Radiocontrast (Iohexol) Removal.International journal of molecular sciences · 2023Article
- The role of kidney injury biomarkers in COVID-19.Renal failure · 2022Review
- Cellular senescence in ischemia/reperfusion injury.Cell death discovery · 2022Review
- From AKI to CKD: Maladaptive Repair and the Underlying Mechanisms.International journal of molecular sciences · 2022Review
- Remote ischemic preconditioning causes transient cell cycle arrest and renal protection by a NF-κB-dependent Sema5B pathway.JCI insight · 2022Article
- Src Family Kinases: A Potential Therapeutic Target for Acute Kidney Injury.Biomolecules · 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI), commonly caused by ischemia-reperfusion injury, has far-reaching health consequences. Despite the significant regenerative capacity of proximal tubular epithelium cells (PTCs), repair frequently fails, leading to the development of chronic kidney disease (CKD). In the last decade, it has been repeatedly demonstrated that dysregulation of the cell cycle can cause injured kidneys to progress to CKD. More precisely, severe AKI causes PTCs to arrest in the G1/S or G2/M phase of the cell cycle, leading to maladaptive repair and a fibrotic outcome. The mechanisms causing these arrests are far from known. The arrest might, at least partially, be attributed to DNA damage since activation of the DNA-damage response pathway leads to cell cycle arrest. Alternatively, cytokine signalling via nuclear factor kappa beta (NF-κβ) and p38-mitogen-activated protein kinase (p38-MAPK) pathways, and reactive oxygen species (ROS) can play a role independent of DNA damage. In addition, only a handful of cell cycle regulators (e.g., p53, p21) have been thoroughly studied during renal repair. Still, why and how PTCs decide to arrest their cell cycle and how this arrest can efficiently be overcome remain open and challenging questions. In this review we will discuss the evidence for cell cycle involvement during AKI and development of CKD together with putative therapeutic approaches.
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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.