ArticleJournal of cellular and molecular medicine2017
Role of endothelial-to-mesenchymal transition induced by TGF-β1 in transplant kidney interstitial fibrosis.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 81 citations in OpenAlex.
- A macrophage-endothelial cell axis in kidney diseases.International urology and nephrology · 2026Review
- Role of microvascular pericyte dysfunction in antibody-mediated rejection following kidney transplantation.Renal failure · 2025Article
- Bidirectional Role of Pericytes in Ischemic Stroke.Brain sciences · 2025Review
- Characterization of gut microbiota and metabolites in renal transplant recipients during COVID-19 and prediction of one-year allograft function.Journal of translational medicine · 2025Article
- Study on the mechanism of OSM participating in myocardial fibrosis by inhibiting TGFβ-induced EndMT of cardiac microvascular endothelial cells through SPARC/SMAD signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- METTL3 Potentiates M2 Macrophage-Driven MMT to Aggravate Renal Allograft Fibrosis via the TGF-β1/Smad3 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- GLP-1 and glucagon receptor dual agonism ameliorates kidney allograft fibrosis by improving lipid metabolism.Frontiers in immunology · 2025Article
- Sorafenib and edaravone protect against renal fibrosis induced by unilateral ureteral obstruction via inhibition of oxidative stress, inflammation, and RIPK-3/MLKL pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Src inhibition modulates AMBRA1-mediated mitophagy to counteract endothelial-to-mesenchymal transition in renal allograft fibrosis.Cell proliferation · 2024Article
- Renal fibroblasts are involved in fibrogenic changes in kidney fibrosis associated with dysfunctional telomeres.Experimental & molecular medicine · 2024Article
- Distinct roles of SOX9 in self-renewal of progenitors and mesenchymal transition of the endothelium.Angiogenesis · 2024Article
- P2 X 7 receptor is a critical regulator of extracellular ATP-induced profibrotic genes expression in rat kidney: implication of transforming growth factor-β/Smad signaling pathway.Purinergic signalling · 2024Article
- Huoxue Jiedu Huayu recipe inhibits macrophage-secreted vascular endothelial growth factor-a on angiogenesis and alleviates renal fibrosis in the contralateral kidneys of unilateral ureteral obstruction rats.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Rictor/mTORC2 signalling contributes to renal vascular endothelial-to-mesenchymal transition and renal allograft interstitial fibrosis by regulating BNIP3-mediated mitophagy.Clinical and translational medicine · 2024Article
- Plasma-derived exosomes contributes to endothelial-to-mesenchymal transition in Moyamoya disease.Heliyon · 2024Article
- Dysregulated lipid metabolism is associated with kidney allograft fibrosis.Lipids in health and disease · 2024Article
- Hexane Fraction ofMolecules (Basel, Switzerland) · 2024Article
- Automated High-Throughput Live Cell Monitoring of Scratch Wound Closure.Biomedical engineering and computational biology · 2024Article
- Macrophage polarization induces endothelium-to-myofibroblast transition in chronic allograft dysfunction.Renal failure · 2023Article
- Esaxerenone Inhibits Renal Angiogenesis and Endothelial-Mesenchymal Transition via the VEGFA and TGF-β1 Pathways in Aldosterone-Infused Mice.International journal of molecular sciences · 2023Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic allograft dysfunction (CAD) induced by kidney interstitial fibrosis is the main cause of allograft failure in kidney transplantation. Endothelial-to-mesenchymal transition (EndMT) may play an important role in kidney fibrosis. We, therefore, undertook this study to characterize the functions and potential mechanism of EndMT in transplant kidney interstitial fibrosis. Proteins and mRNAs associated with EndMT were examined in human umbilical vein endothelial cells (HUVECs) treated with transforming growth factor-beta1 (TGF-β1) at different doses or at different intervals with western blotting, qRT-PCR and ELISA assays. Cell motility and migration were evaluated with motility and migration assays. The mechanism of EndMT induced by TGF-β1 was determined by western blotting analysis of factors involved in various canonical and non-canonical pathways. In addition, human kidney tissues from control and CAD group were also examined for these proteins by HE, Masson's trichrome, immunohistochemical, indirect immunofluorescence double staining and western blotting assays. TGF-β1 significantly promoted the development of EndMT in a time-dependent and dose-dependent manner and promoted the motility and migration ability of HUVECs. The TGF-β/Smad and Akt/mTOR/p70S6K signalling pathways were found to be associated with the pathogenesis of EndMT induced by TGF-β1, which was also proven in vivo by the analysis of specimens from the control and CAD groups. EndMT may promote transplant kidney interstitial fibrosis by targetting the TGF-β/Smad and Akt/mTOR/p70S6K signalling pathways, and hence, result in the development of CAD in kidney transplant recipients.
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