ReviewKidney diseases (Basel, Switzerland)2016
Signaling Crosstalk between Tubular Epithelial Cells and Interstitial Fibroblasts after Kidney Injury.
Review in Kidney diseases (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 115 citations in OpenAlex.
- Ubiquitin-specific protease 11 facilitates the activation and proliferation of renal interstitial fibroblasts through epidermal growth factor receptor signaling pathways.Renal failure · 2026Article
- A model for Crohn's disease post-ileal resection fibrosis development using human ileal enteroids and myofibroblasts.Frontiers in physiology · 2026Article
- Protecting kidney function: from mechanisms to therapeutic targets and traditional Chinese medicine.Renal failure · 2025Review
- Single-cell RNA sequencing revealed the association between proximal tubular epithelial cells and renal interstitial cells in chronic kidney disease progression.Scientific reports · 2025Article
- Injured tubule derived CCN1 exacerbates renal congestion-mediated acute kidney injury and fibrosis.Scientific reports · 2025Article
- Injured tubular epithelia-derived CCN1 promotes the mobilization of fibroblasts toward injury sites after kidney injury.iScience · 2025Article
- Emerging roles of exosomes in the diagnosis and treatment of kidney diseases.Frontiers in pharmacology · 2025Review
- Urinary exosomes as promising biomarkers for early kidney disease detection.American journal of clinical and experimental urology · 2025Review
- Exosomes on the development and progression of renal fibrosis.Cell proliferation · 2024Review
- Renal tubular epithelial cells response to injury in acute kidney injury.EBioMedicine · 2024Review
- Myocardin-Related Transcription Factor Mediates Epithelial Fibrogenesis in Polycystic Kidney Disease.Cells · 2024Article
- Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics.Cell death discovery · 2024Review
- Cell-cell communication in kidney fibrosis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Review
- Mechanosensitive Cation Channel Piezo1 Is Involved in Renal Fibrosis Induction.International journal of molecular sciences · 2024Review
- The role of intercellular communication in diabetic nephropathy.Frontiers in immunology · 2024Review
- Kidney tubular epithelial cells control interstitial fibroblast fate by releasing TNFAIP8-encapsulated exosomes.Cell death & disease · 2023Article
- Hedgehog-induced ZFYVE21 promotes chronic vascular inflammation by activating NLRP3 inflammasomes in T cells.Science signaling · 2023Article
- A therapeutic target for CKD: activin A facilitates TGFβ1 profibrotic signaling.Cellular & molecular biology letters · 2023Article
- Crosstalk between proximal tubular epithelial cells and other interstitial cells in tubulointerstitial fibrosis after renal injury.Frontiers in endocrinology · 2023Review
- Blocking connexin 43 hemichannel-mediated ATP release reduces communication within and between tubular epithelial cells and medullary fibroblasts in a model of diabetic nephropathy.Diabetic medicine : a journal of the British Diabetic Association · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundA wide variety of kidney diseases ultimately lead to tubulointerstitial damage. The initial site of injury is usually the renal tubules, with activation of fibroblasts occurring later. Self-limited disease is characterized by transient cellular activation with timed deactivation and ultimately a return to normal functioning, whereas sustained responses characterize chronic disease and the development of irreversible fibrosis. The underlying molecular and cellular mechanisms of this cascade of events remain an area of active research. Current data overwhelmingly support a role for crosstalk between the tubular epithelium and the interstitial fibroblast that mediates both repair/regeneration and progressive disease. This epithelial-mesenchymal communication (EMC) is regulated by a variety of soluble ligands binding to cell surface receptors to induce intracellular signaling events. SUMMARY: EMC is an important mechanism whereby tubular epithelium and fibroblasts/mesenchymal cells crosstalk to affect renal physiology and pathology. Numerous soluble factors such as sonic hedgehog, Wnt ligands, transforming growth factor-β, hepatocyte growth factor, connective tissue growth factor, and angiotensin II all participate in bidirectional EMC. Recent studies have also identified exosomes as a vehicle to mediate EMC during kidney injury. In general, while the short-term activity of EMC factors is renoprotective, prolonged activation of these factors leads to chronic disease and fibrosis. KEY MESSAGES: The discovery of a complex and intricate system of communication between tubular cells and fibroblasts is a new paradigm in our understanding of renal fibrosis. An appreciation of both their regenerative and pathologic functions will inform the development and use of targeted therapeutic interventions.
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