ReviewCell death & disease2018
Renal tubular epithelial cells: the neglected mediator of tubulointerstitial fibrosis after injury.
Review in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.
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Who cites it
154 citing papers in PubMed, 238 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
- Lactylation-dependent DDX18 nucleolar escape regulates CD44 mRNA stability to drive fibrotic progression in kidney injury.The Journal of clinical investigation · 2026Article
- SMOC2 promotes partial epithelial-mesenchymal transition and maladaptive repair in renal tubular epithelial cells.JCI insight · 2026Article
- Shengqingjiangzhuo Capsules Alleviates Renal Fibrosis by Targeting Glomerular Endothelial Cells Exosome miR-31-5p/HO-1 to Suppress Tubular Epithelial Cells Ferroptosis.Clinical and experimental pharmacology & physiology · 2026Article
- Interferon-λ drives renal fibrosis by coordinating epithelial-fibroblast crosstalk.The Journal of experimental medicine · 2026Article
- Targeting NAT10 with Remodelin reshapes the pro-fibrotic microenvironment in renal fibrogenesisActa pharmaceutica Sinica. B · 2026Article
- Article
- A TGF-β1/LEF1/β-catenin/JLP network motif regulates autophagy and tubule injury in renal fibrosis.JCI insight · 2026Article
- Targeting Cathepsin B with p-coumaric acid rescues WWP1-dependent proteasomal degradation of NLRP3 in hyperuricemic nephropathy.Molecular medicine (Cambridge, Mass.) · 2026Article
- Article
- Multi-omics profiling reveals EMT-driven fibroblast activation in the renal injury niche.Cellular and molecular life sciences : CMLS · 2026Article
- Renal fibrosis is induced by hyperactive Wnt/β-catenin pathway via microbial-mediated tryptophan metabolism-driven AhR signaling in rodents and humans.Cellular and molecular life sciences : CMLS · 2026Article
- MicroRNA-451 Modulates Autophagy-Related Signaling with Relevance to Renal Fibrosis in an Accelerated Mouse Model of Diabetic Kidney Disease.Current issues in molecular biology · 2026Article
- Empagliflozin protected kidney function in CKD rat through suppressing hypoxic and fibrotic signalings mediated inflammation and EMT.Histology and histopathology · 2026Article
- egr1 and egr4 regulate zebrafish renal regeneration by promoting foxm1 expression.Journal of molecular cell biology · 2026Article
- A comprehensive approach to elucidating the pathophysiology of kidney fibrosis based on extracellular vesicle proteomics.Frontiers in physiology · 2026Article
- Bruceine A attenuates renal tubulointerstitial fibrosis by inhibiting the Wnt7a/PI3K/AKT pathway.Frontiers in pharmacology · 2026Article
- Cellular senescence of renal tubular epithelial cells in diabetic kidney disease: emerging mechanisms and targeted interventions.Frontiers in cell and developmental biology · 2026Review
- Dedifferentiated proximal tubular epithelial cells in diabetic kidney disease: pathogenic roles, repair potential, and therapeutic implications.Frontiers in endocrinology · 2026Review
- Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.Frontiers in medicine · 2026Review
94 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal fibrosis, especially tubulointerstitial fibrosis, is the inevitable outcome of all progressive chronic kidney diseases (CKDs) and exerts a great health burden worldwide. For a long time, interests in renal fibrosis have been concentrated on fibroblasts and myofibroblasts. However, in recent years, growing numbers of studies have focused on the role of tubular epithelial cells (TECs). TECs, rather than a victim or bystander, are probably a neglected mediator in renal fibrosis, responding to a variety of injuries. The maladaptive repair mechanisms of TECs may be the key point in this process. In this review, we will focus on the role of TECs in tubulointerstitial fibrosis. We will follow the fate of a tubular cell and depict the intracellular changes after injury. We will then discuss how the repair mechanism of tubular cells becomes maladaptive, and we will finally discuss the intercellular crosstalk in the interstitium that ultimately proceeds tubulointerstitial fibrosis.
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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 Socratic graph.