ReviewInternational journal of molecular sciences2021
Tubular Cell Cycle Response upon AKI: Revising Old and New Paradigms to Identify Novel Targets for CKD Prevention.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 32 citations in OpenAlex.
- From AKI to CKD mechanisms of maladaptive repair and disease progression.International urology and nephrology · 2026Review
- Pharmacologic disruption of HuR-RNA interactions prevents maladaptive tubular repair and AKI-to-CKD progression.American journal of physiology. Renal physiology · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Sex-dependent transcriptional responses and druggable targets in gentamicin-induced nephrotoxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Review
- Distinct p21 dynamics drive alternative routes to whole-genome duplication through a common CDK4/6-dependent polyploid G0 state.bioRxiv : the preprint server for biology · 2026Article
- The Effect of Renal Ischemia/Reperfusion on the Renal Expression of Epithelial Sodium Channels in Rat: Possible Role of Neural Precursor Cell-Expressed Developmentally Down-Regulated Protein (Nedd4-2).Kidney & blood pressure research · 2026Article
- Reappraisal of profibrotic phenotype and cell-cycle state of renal tubular epithelium after ischemia-reperfusion injury.PloS one · 2026Article
- Noncanonical function of Pannexin1 promotes cellular senescence and renal fibrosis post-acute kidney injury.Nature communications · 2025Article
- Cellular senescence in renal ischemia-reperfusion injury.Chinese medical journal · 2025Review
- 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
- Molecular mechanisms and therapeutic advances of peritubular capillary neogenesis in acute kidney injury.Frontiers in molecular biosciences · 2025Review
- Acute kidney injury through a metabolic lens: pathological reprogramming mechanisms and clinical translation potential.Frontiers in physiology · 2025Review
- Article
- Nanotherapeutic kidney cell-specific targeting to ameliorate acute kidney injury.Kidney international · 2024Article
- SNORD3A Regulates STING Transcription to Promote Ferroptosis in Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Hazel Leaf Polyphenol Extract Alleviated Cisplatin-Induced Acute Kidney Injury by Reducing Ferroptosis through Inhibiting Hippo Signaling.Molecules (Basel, Switzerland) · 2024Article
- Advances and potential of regenerative medicine in pediatric nephrology.Pediatric nephrology (Berlin, Germany) · 2024Review
- Evaluation of Selected Markers in Kidneys of Cynomolgus Monkey (Comparative medicine · 2023Article
- The Therapeutic Potential of CDK4/6 Inhibitors, Novel Cancer Drugs, in Kidney Diseases.International journal of molecular sciences · 2023Review
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
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is characterized by a rapid deterioration of kidney function, representing a global healthcare concern. In addition, AKI survivors frequently develop chronic kidney disease (CKD), contributing to a substantial proportion of disease burden globally. Yet, over the past 30 years, the burden of CKD has not declined to the same extent as many other important non-communicable diseases, implying a substantial deficit in the understanding of the disease progression. The assumption that the kidney response to AKI is based on a high proliferative potential of proximal tubular cells (PTC) caused a critical confounding factor, which has led to a limited development of strategies to prevent AKI and halt progression toward CKD. In this review, we discuss the latest findings on multiple mechanisms of response related to cell cycle behavior of PTC upon AKI, with a specific focus on their biological relevance. Collectively, we aim to (1) provide a new perspective on interpreting cell cycle progression of PTC in response to damage and (2) discuss how this knowledge can be used to choose the right therapeutic window of treatment for preserving kidney function while avoiding CKD progression.
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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.