ArticleNature medicine2015
Epithelial-to-mesenchymal transition induces cell cycle arrest and parenchymal damage in renal fibrosis.
Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 569 papers, 1 of them a synthesis that pooled it.
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Who cites it
569 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Beneficial effects of cell-derived exosomes on diabetic nephropathy: a systematic review and meta-analysis of preclinical evidence.Acta diabetologica · 2025Pooled it
- From AKI to CKD mechanisms of maladaptive repair and disease progression.International urology and nephrology · 2026Review
- 3D tissue model to patient atlas: dynamic network topology reveals PDAC chemoresistance bottlenecks.NPJ systems biology and applications · 2026Article
- Integrated single-cell and bulk transcriptomic analysis identifies epithelial cell-related biomarkers and immune subtypes in focal segmental glomerulosclerosis.International urology and nephrology · 2026Article
- The role of senescence in kidney ageing, injury and fibrosis.Nature reviews. Nephrology · 2026Review
- SMOC2 promotes partial epithelial-mesenchymal transition and maladaptive repair in renal tubular epithelial cells.JCI insight · 2026Article
- EPLIN stabilizes cell-cell adhesion complexes to facilitate TGF-β1-induced fibroblastic differentiation of human periodontal ligament stem cells.Stem cells (Dayton, Ohio) · 2026Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Article
- Twist Family BHLH Transcription Factor 1 orchestrates hypoxia-lactate crosstalk to bridge glycolytic flux and tubular maladaptation in fibrotic kidneys.Molecular biomedicine · 2026Article
- Article
- Research Progress on the Treatment of Renal Injury with Esculetin: Multi-Target Pharmacological Mechanism and Clinical Translation Prospect.International journal of molecular sciences · 2026Review
- Article
- Article
- Integrating Metabolomics and Network Pharmacology to Reveal the Mechanism of Thymoquinone Alleviating Renal Interstitial Fibrosis in UUO Mice.International journal of molecular sciences · 2026Article
- Renal Tubular Epithelial Cells as Central Hubs of Kidney Disease.Diagnostics (Basel, Switzerland) · 2026Review
- Single-cell morphodynamical trajectories enable prediction of gene expression accompanying cell state change.Cell systems · 2026Article
- Integrated Single-Cell Whole-Genome Sequencing and Spatial Transcriptomics Reveal Intratumoral Heterogeneity in Ovarian Cancer.Cancer research communications · 2026Article
- Phillygenin, a Plant-Derived Lignan, Attenuates Renal Inflammation, Fibrosis, and Pyroptosis in a Unilateral Ureteral Obstruction Model.Nutrients · 2026Article
- Urinary Microbiome Characteristics in Kidney Transplant Recipients and Their Clinical Implications: A Narrative Review.Annals of transplantation · 2026Review
509 more citing papers are in PubMed but not listed here.
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14 authors.
Funding
Abstract
Kidney fibrosis is marked by an epithelial-to-mesenchymal transition (EMT) of tubular epithelial cells (TECs). Here we find that, during renal fibrosis, TECs acquire a partial EMT program during which they remain associated with their basement membrane and express markers of both epithelial and mesenchymal cells. The functional consequence of the EMT program during fibrotic injury is an arrest in the G2 phase of the cell cycle and lower expression of several solute and solvent transporters in TECs. We also found that transgenic expression of either Twist1 (encoding twist family bHLH transcription factor 1, known as Twist) or Snai1 (encoding snail family zinc finger 1, known as Snail) expression is sufficient to promote prolonged TGF-β1-induced G2 arrest of TECs, limiting the cells' potential for repair and regeneration. In mouse models of experimentally induced renal fibrosis, conditional deletion of Twist1 or Snai1 in proximal TECs resulted in inhibition of the EMT program and the maintenance of TEC integrity, while also restoring cell proliferation, dedifferentiation-associated repair and regeneration of the kidney parenchyma and attenuating interstitial fibrosis. Thus, inhibition of the EMT program in TECs during chronic renal injury represents a potential anti-fibrosis therapy.
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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.