ArticleFASEB bioAdvances2023
Exosomes from tubular epithelial cells undergoing epithelial-to-mesenchymal transition promote renal fibrosis by M1 macrophage activation.
Article in FASEB bioAdvances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Diagnostic and Therapeutic Roles of Extracellular Vesicles in Chronic Kidney Disease: A Systematic Review.Journal of extracellular vesicles · 2026Pooled it
- Mitochondrial dysfunction of renal tubular epithelial cells in chronic kidney disease-associated fibrosis: from organelle homeostasis to multicellular remodeling.Molecular biology reports · 2026Review
- Macrophage heterogeneity in organ fibrosis in the era of single-cell omics.Molecular biology reports · 2026Review
- The Lactate-lactylation circuitry in kidney fibrosis: cellular crosstalk from tubular metabolic reprogramming to macrophage effector functions.Seminars in immunopathology · 2026Review
- Leveraging extracellular vesicle biology for novel tests and therapeutics for kidney fibrosis.Clinical and translational medicine · 2026Review
- The role of extracellular vesicles in kidney disease progression.Kidney research and clinical practice · 2026Article
- Meta-analysis study of the therapeutic impact of Mesenchymal stem cells derived exosomes for chronic kidney diseases.Biochemistry and biophysics reports · 2025Article
- Extracellular Vesicles from Induced Mesenchymal Stem Cells Inhibit Acute Kidney Injury to Chronic Kidney Disease Transition.International journal of stem cells · 2025Article
- Tubular-Cell-Derived Extracellular Vesicle miR-491-3p Aggravates Renal Ischemia-Reperfusion Injury by Inhibiting Macrophage SIRT1-Mediated Notch Intracellular Domain Deacetylation-Driven Ubiquitin-Proteasome Degradation.Research (Washington, D.C.) · 2025Article
- Emerging roles of exosomes in the diagnosis and treatment of kidney diseases.Frontiers in pharmacology · 2025Review
- Exosomes on the development and progression of renal fibrosis.Cell proliferation · 2024Review
- Renal tubular epithelial cell quality control mechanisms as therapeutic targets in renal fibrosis.Journal of pharmaceutical analysis · 2024Review
- Tonabersat suppresses priming/activation of the NOD-like receptor protein-3 (NLRP3) inflammasome and decreases renal tubular epithelial-to-macrophage crosstalk in a model of diabetic kidney disease.Cell communication and signaling : CCS · 2024Article
- Article
- The Dual Role of Neutrophil Extracellular Traps (NETs) in Sepsis and Ischemia-Reperfusion Injury: Comparative Analysis across Murine Models.International journal of molecular sciences · 2024Article
- Fibrosis in Chronic Kidney Disease: Pathophysiology and Therapeutic Targets.Journal of clinical medicine · 2024Review
- Unraveling the Multifaceted Roles of Extracellular Vesicles: Insights into Biology, Pharmacology, and Pharmaceutical Applications for Drug Delivery.International journal of molecular sciences · 2023Review
- Exosomes from tubular epithelial cells undergoing epithelial-to-mesenchymal transition promote renal fibrosis by M1 macrophage activation.FASEB bioAdvances · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kidney fibrosis is the common final pathway of chronic kidney disease (CKD), and it is distinguished by inflammation, mesenchymal transition with myofibroblast formation, and epithelial-to-mesenchymal transition (EMT). Macrophages are protuberant inflammatory cells in the kidney, and their roles are dependent on their phenotypes. However, it remains unclear whether tubular epithelial cells (TECs) undergoing EMT can influence the phenotypes of macrophages and the underlying mechanisms during the development of kidney fibrosis. Here, we investigated the characteristics of TECs and macrophages during kidney fibrosis with a focus on EMT and inflammation. We found that the coculture of exosomes from transforming growth factor-beta (TGF-β)-induced TECs with macrophages induced macrophage M1 polarization, while exosomes from TECs without TGF-β stimulation or stimulation with TGF-β alone did not induce an increase in M1 macrophage-related markers. Notably, TECs induced to undergo EMT by TGF-β treatment released more exosomes than the other groups. Furthermore, it is noteworthy that when we injected exosomes from TECs undergoing EMT into mice, in addition to the high level of inflammatory response and the activation of M1 macrophages, the indicators of EMT and renal fibrosis in mouse kidney tissue were correspondingly elevated. In summary, exosomes from TECs undergoing EMT by TGF-β treatment induced M1 polarization and led to a positive feedback effect for further EMT and the development of renal fibrosis. Therefore, the obstacle to the release of such exosomes may be a novel therapeutic strategy for CKD.
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