ReviewClinical and experimental nephrology2013
Role of the endothelial-to-mesenchymal transition in renal fibrosis of chronic kidney disease.
Review in Clinical and experimental nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 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.
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Who cites it
95 citing papers in PubMed, 164 citations in OpenAlex.
- Wound Healing and Angiogenic Profiling of Dermal Endothelial Cells Isolated From People With Type 2 Diabetes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Bufalin-Induced Epithelial-to-Mesenchymal Transition in Kidney Epithelial Cells.Cell biology international · 2025Article
- Exploring disulfiram mechanisms in renal fibrosis: insights from biological data and computational approaches.Frontiers in pharmacology · 2025Article
- Targeting E3 ubiquitin ligases: a new frontier in idiopathic pulmonary fibrosis treatment.Frontiers in immunology · 2025Review
- Novel dysregulated long non-coding RNAs in the acute kidney injury-to-chronic kidney diseases transition unraveled by transcriptomic analysis.Pharmacology research & perspectives · 2024Article
- A genetically inducible endothelial niche enables vascularization of human kidney organoids with multilineage maturation and emergence of renin expressing cells.Kidney international · 2024Article
- Endothelial-mesenchymal transition in skeletal muscle: Opportunities and challenges from 3D microphysiological systems.Bioengineering & translational medicine · 2024Review
- Circulating neutrophil extracellular trap remnants as a biomarker to predict outcomes in lupus nephritis.Lupus science & medicine · 2024Article
- Possible mechanisms of SARS-CoV-2-associated myocardial fibrosis: reflections in the post-pandemic era.Frontiers in microbiology · 2024Review
- The molecular mechanisms of peptidyl-prolylFrontiers in pharmacology · 2024Review
- Genetically engineering endothelial niche in human kidney organoids enables multilineage maturation, vascularization and de novo cell types.bioRxiv : the preprint server for biology · 2023Article
- Non-Haemodynamic Mechanisms Underlying Hypertension-Associated Damage in Target Kidney Components.International journal of molecular sciences · 2023Review
- Dual soluble epoxide hydrolase inhibitor - farnesoid X receptor agonist interventional treatment attenuates renal inflammation and fibrosis.Frontiers in immunology · 2023Article
- Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial Dysfunction.Marine drugs · 2022Article
- Pharmacological and Chemical Potential ofPlants (Basel, Switzerland) · 2022Review
- Adenosine/adenosine type 1 receptor signaling pathway did not play dominant roles on the influence of sodium-glucose cotransporter 2 inhibitor in the kidney of bovine serum albumin-overloaded streptozotocin-induced diabetic mice.Journal of diabetes investigation · 2022Article
- Endothelial ETS1 inhibition exacerbate blood-brain barrier dysfunction in multiple sclerosis through inducing endothelial-to-mesenchymal transition.Cell death & disease · 2022Article
- Improving the residual risk of renal and cardiovascular outcomes in diabetic kidney disease: A review of pathophysiology, mechanisms, and evidence from recent trials.Diabetes, obesity & metabolism · 2022 · on this mapReview
- Twist1 regulates macrophage plasticity to promote renal fibrosis through galectin-3.Cellular and molecular life sciences : CMLS · 2022Article
- Chemokine (C-C Motif) Ligand 8 and Tubulo-Interstitial Injury in Chronic Kidney Disease.Cells · 2022Article
35 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
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
All types of progressive chronic kidney disease (CKD) inevitably induce renal fibrosis, the hallmark of which is the activation and accumulation of a large number of matrix-producing fibroblasts or myofibroblasts. The activated fibroblasts or myofibroblasts are derived from diverse origins, such as residential fibroblasts, vascular pericytes, epithelial-to-mesenchymal transition (EMT), and bone marrow (circulating fibrocytes). Recently, endothelial-to-mesenchymal transition (EndMT) or endothelial-to-myofibroblast transition has also been suggested to promote fibrosis and is recognized as a novel mechanism for the generation of myofibroblasts. Similar to EMT, during EndMT, endothelial cells lose their adhesion and apical-basal polarity to form highly invasive, migratory, spindle-shaped, elongated mesenchymal cells. More importantly, biochemical changes accompany these distinct changes in cell polarity and morphology, including the decreased expression of endothelial markers and the acquisition of mesenchymal markers. This review highlights evidence supporting the important role of EndMT in the development of renal fibrosis in CKD and its underlying mechanisms, including novel biological significance of microRNA regulation.
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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.