ArticleNature communications2018
Endocycle-related tubular cell hypertrophy and progenitor proliferation recover renal function after acute kidney injury.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.
What it found
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Who cites it
141 citing papers in PubMed, 261 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
- Single-cell spatial mapping of human kidney development implicates the microenvironment in guiding cell fate decisions.Nature genetics · 2026Article
- Article
- Epithelial cell fusion is required for tissue repair following UV-A irradiation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Growth under pressure: The pros and cons of polyploidy induced by stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Review
- The HDAC1 inhibitor attenuates renal ischemia-reperfusion injury via dual epigenetic modulation of p53 and macrophage NF-κB pathways.Cell biology and toxicology · 2026Article
- Clonal embeddings allow exploratory analysis of lineage-resolved single-cell data.bioRxiv : the preprint server for biology · 2026Article
- Morphological abnormalities in the ureter of type XVII collagen-deficient mice.Scientific reports · 2026Article
- Deletion of exocyst component 5 suppresses repair of injured kidney by limiting cell proliferation.Cell death discovery · 2026Article
- Multifactorial chronic kidney disease and the kidney capacity-workload balance.Nature reviews. Nephrology · 2026Review
- egr1 and egr4 regulate zebrafish renal regeneration by promoting foxm1 expression.Journal of molecular cell biology · 2026Article
- Lineage tracing reveals KSPFrontiers in cell and developmental biology · 2026Article
- Toward Combinatorial Strategies to Improve Proximal Tubule Recovery Following Acute Kidney Injury.Seminars in nephrology · 2026Review
- Renovascular Disease and Its Impact on Endogenous Kidney Repair: Stem/Progenitor Cells.Stem cells international · 2026Review
- Reappraisal of profibrotic phenotype and cell-cycle state of renal tubular epithelium after ischemia-reperfusion injury.PloS one · 2026Article
- Modeling kidney fibrosis and tubular regeneration in iPSC-derived kidney organoids.Stem cell research & therapy · 2025Article
- Regenerative Versus Nonregenerative Repair of the Renal Medulla After Reversal of Ureteral Obstruction.Seminars in nephrology · 2025Review
- Hepatocytes as Model for Investigating Natural Senotherapeutic Compounds and Their Effects on Cell Cycle Dynamics and Genome Stability.International journal of molecular sciences · 2025Review
- Tubular Cell Polyploidy and AKI-to-CKD Transition.Journal of the American Society of Nephrology : JASN · 2025Article
- Macrophage-Derived Type 1 IFN, Renal Tubular Epithelial Cell Polyploidization, and AKI-to-CKD Transition.Journal of the American Society of Nephrology : JASN · 2025Article
81 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is considered largely reversible based on the capacity of surviving tubular cells to dedifferentiate and replace lost cells via cell division. Here we show by tracking individual tubular cells in conditional Pax8/Confetti mice that kidney function is recovered after AKI despite substantial tubular cell loss. Cell cycle and ploidy analysis upon AKI in conditional Pax8/FUCCI2aR mice and human biopsies identify endocycle-mediated hypertrophy of tubular cells. By contrast, a small subset of Pax2+ tubular progenitors enriches via higher stress resistance and clonal expansion and regenerates necrotic tubule segments, a process that can be enhanced by suitable drugs. Thus, renal functional recovery upon AKI involves remnant tubular cell hypertrophy via endocycle and limited progenitor-driven regeneration that can be pharmacologically enhanced.
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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.