ArticleEMBO molecular medicine2015
Caveolin-1 deficiency induces a MEK-ERK1/2-Snail-1-dependent epithelial-mesenchymal transition and fibrosis during peritoneal dialysis.
Article in EMBO molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers, 1 of them a synthesis that pooled it.
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.
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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.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Mechanisms of Peritoneal Fibrosis: Focus on Immune Cells-Peritoneal Stroma Interactions.Frontiers in immunology · 2021Pooled it
- Loss of Gαq reshapes fibroblast traits and drives tumor-stroma remodeling in oral cancer progression.EMBO reports · 2026Article
- Endosome traffic in rheumatic diseases: mechanistic insights and therapeutic opportunities.Nature reviews. Rheumatology · 2026Review
- The role of Caveolin-1 in tumor-derived extracellular vesicle biology and its implications.Frontiers in cell and developmental biology · 2025Review
- Metastasis-associated fibroblasts in peritoneal surface malignancies.British journal of cancer · 2024Review
- Effect of cellular senescence on the response of human peritoneal mesothelial cells to TGF-β.Scientific reports · 2024Article
- Cavin-2 promotes fibroblast-to-myofibroblast trans-differentiation and aggravates cardiac fibrosis.ESC heart failure · 2024Article
- Caveolae Mechanotransduction at the Interface between Cytoskeleton and Extracellular Matrix.Cells · 2023Review
- Role of Ferroptosis in Regulating the Epithelial-Mesenchymal Transition in Pulmonary Fibrosis.Biomedicines · 2023Review
- A review of research progress on mechanisms of peritoneal fibrosis related to peritoneal dialysis.Frontiers in physiology · 2023Review
- MAPKs in the early steps of senescence implemEMTation.Frontiers in cell and developmental biology · 2023Article
- Interplay between mechanics and signalling in regulating cell fate.Nature reviews. Molecular cell biology · 2022Review
- Fibrosis of Peritoneal Membrane as Target of New Therapies in Peritoneal Dialysis.International journal of molecular sciences · 2022Review
- Article
- Silencing COX-2 blocks PDK1/TRAF4-induced AKT activation to inhibit fibrogenesis during skeletal muscle atrophy.Redox biology · 2021Article
- Cellular and molecular events of inflammation induced transdifferentiation (EMT) and regeneration (MET) in mesenteric mesothelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
- Review
- NMDA receptor-mediated CaMKII/ERK activation contributes to renal fibrosis.BMC nephrology · 2020Article
- Caveolin1 and YAP drive mechanically induced mesothelial to mesenchymal transition and fibrosis.Cell death & disease · 2020Article
- Recent advances in understanding the role of hypoxia-inducible factor 1α in renal fibrosis.International urology and nephrology · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peritoneal dialysis (PD) is a form of renal replacement therapy whose repeated use can alter dialytic function through induction of epithelial-mesenchymal transition (EMT) and fibrosis, eventually leading to PD discontinuation. The peritoneum from Cav1-/- mice showed increased EMT, thickness, and fibrosis. Exposure of Cav1-/- mice to PD fluids further increased peritoneal membrane thickness, altered permeability, and increased the number of FSP-1/cytokeratin-positive cells invading the sub-mesothelial stroma. High-throughput quantitative proteomics revealed increased abundance of collagens, FN, and laminin, as well as proteins related to TGF-β activity in matrices derived from Cav1-/- cells. Lack of Cav1 was associated with hyperactivation of a MEK-ERK1/2-Snail-1 pathway that regulated the Smad2-3/Smad1-5-8 balance. Pharmacological blockade of MEK rescued E-cadherin and ZO-1 inter-cellular junction localization, reduced fibrosis, and restored peritoneal function in Cav1-/- mice. Moreover, treatment of human PD-patient-derived MCs with drugs increasing Cav1 levels, as well as ectopic Cav1 expression, induced re-acquisition of epithelial features. This study demonstrates a pivotal role of Cav1 in the balance of epithelial versus mesenchymal state and suggests targets for the prevention of fibrosis during PD.
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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.