ArticlePloS one2014
Collective epithelial migration drives kidney repair after acute injury.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 34 citations in OpenAlex.
- Lactylation-dependent DDX18 nucleolar escape regulates CD44 mRNA stability to drive fibrotic progression in kidney injury.The Journal of clinical investigation · 2026Article
- Proteasome-dependent cytoskeleton disruption during Leptospira interrogans infection induces aberrant collective cell migration.PLoS pathogens · 2026Article
- Modeling Podocyte Ontogeny and Podocytopathies with the Zebrafish.Journal of developmental biology · 2023Review
- Advances in Understanding the Genetic Mechanisms of Zebrafish Renal Multiciliated Cell Development.Journal of developmental biology · 2022Review
- Histone Deacetylases Cooperate with NF-κB to Support the Immediate Migratory Response after Zebrafish Pronephros Injury.International journal of molecular sciences · 2022Article
- Control of Directed Cell Migration after Tubular Cell Injury by Nucleotide Signaling.International journal of molecular sciences · 2022Article
- Unexpected localization of AQP3 and AQP4 induced by migration of primary cultured IMCD cells.Scientific reports · 2021Article
- Migration of Human Renal Tubular Epithelial Cells in Response to Physiological Electric Signals.Frontiers in cell and developmental biology · 2021Article
- Advances in understanding vertebrate nephrogenesis.Tissue barriers · 2020Article
- The Effect of Shen Qi Wan Medicated Serum on NRK-52E Cells Proliferation and Migration by Targeting Aquaporin 1 (AQP1).Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Prostaglandin signaling regulates renal multiciliated cell specification and maturation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Mind the gap: renal tubule responses to injury and the role of Cxcl12 and Myc.Annals of translational medicine · 2019Article
- Nephron repair: powered by anaerobic energy metabolism.Annals of translational medicine · 2019Article
- The NaThe Journal of physiology · 2019Article
- Article
- CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury.Nature communications · 2018Article
- HIF stabilization inhibits renal epithelial cell migration and is associated with cytoskeletal alterations.Scientific reports · 2018Article
- Precise Cellular Ablation Approach for Modeling Acute Kidney Injury in Developing Zebrafish.Journal of visualized experiments : JoVE · 2017Article
- Caudal migration and proliferation of renal progenitors regulates early nephron segment size in zebrafish.Scientific reports · 2016Article
- Nephrotoxin Microinjection in Zebrafish to Model Acute Kidney Injury.Journal of visualized experiments : JoVE · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is a common and significant medical problem. Despite the kidney's remarkable regenerative capacity, the mortality rate for the AKI patients is high. Thus, there remains a need to better understand the cellular mechanisms of nephron repair in order to develop new strategies that would enhance the intrinsic ability of kidney tissue to regenerate. Here, using a novel, laser ablation-based, zebrafish model of AKI, we show that collective migration of kidney epithelial cells is a primary early response to acute injury. We also show that cell proliferation is a late response of regenerating kidney epithelia that follows cell migration during kidney repair. We propose a computational model that predicts this temporal relationship and suggests that cell stretch is a mechanical link between migration and proliferation, and present experimental evidence in support of this hypothesis. Overall, this study advances our understanding of kidney repair mechanisms by highlighting a primary role for collective cell migration, laying a foundation for new approaches to treatment of AKI.
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.