ReviewKidney international2017
Progression of chronic kidney disease: too much cellular talk causes damage.
Review in Kidney international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
93 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.
- Potential Therapeutic Effects of Natural Plant Compounds in Kidney Disease.Molecules (Basel, Switzerland) · 2021Pooled it
- Sickle Cell Disease and Kidney Injury: Circulating Uromodulin Allows Early Tissue Specific Diagnosis and Monitoring of Treatment.American journal of hematology · 2026Article
- Magnesium Attenuates Renal Senescence and Fibrosis With Reduced DNA Damage Response and H3K4me3 Enrichment at the p16FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- JUNB transcriptional regulation of KRT20 via ITGB1 activates PI3K/AKT signaling pathway against fibrosis-induced by renal injury.Biology direct · 2026Article
- Shedding light on the role of extracellular vesicles in renal fibrosis.Fundamental research · 2026Review
- Residual Renal Risk in Diabetic Nephropathy Despite Contemporary Therapies.Journal of clinical medicine · 2026Review
- Critical role of transcription factor SOX4 in tubular epithelial cell dedifferentiation and fibroblast activation during kidney fibrosis.Kidney international · 2026Article
- Article
- Inhibition of the YAP-E2F2-FGF2 axis in renal tubular cells ameliorates renal fibrosis in chronic kidney disease.Science China. Life sciences · 2026Article
- Comprehensive analysis of pyroptosis-related gene signatures in renal fibrosis.Clinical and experimental nephrology · 2025Article
- Chemical exchange saturation transfer magnetic resonance imaging of the kidney: applications and challenges.Abdominal radiology (New York) · 2025Review
- Histone modification-mediated epigenetic regulation in AKI-to-CKD transition: a cell-type-specific perspective.Journal of translational medicine · 2025Review
- Inhibition of eCIRP attenuates PANoptosis and renal fibrosis.American journal of physiology. Renal physiology · 2025Article
- Fibroblast activation and heterogeneity in fibrotic disease.Nature reviews. Nephrology · 2025Review
- Multimodal spatial transcriptomic characterization of mouse kidney injury and repair.Nature communications · 2025Article
- Serum Levels of NBiomedicines · 2025Article
- Injured tubule derived CCN1 exacerbates renal congestion-mediated acute kidney injury and fibrosis.Scientific reports · 2025Article
- Ablation of macrophage transcriptional factor FoxO1 protects against ischemia-reperfusion injury-induced acute kidney injury.Acta pharmaceutica Sinica. B · 2025Article
- Altered renal vascular patterning reduces ischemic kidney injury and limits age-associated vascular loss.American journal of physiology. Renal physiology · 2025Article
- Injured tubular epithelia-derived CCN1 promotes the mobilization of fibroblasts toward injury sites after kidney injury.iScience · 2025Article
33 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
3 authors at 2 institutions in 1 country.
Funding
Abstract
Tubulointerstitial fibrosis, tubular atrophy, and peritubular capillary rarefaction are major hallmarks of chronic kidney disease. The tubulointerstitium consists of multiple cell components including tubular epithelial, mesenchymal (fibroblasts and pericytes), endothelial, and inflammatory cells. Crosstalk among these cell components is a key component in the pathogenesis of this complex disease. After severe or recurrent injury, the renal tubular epithelial cells undergo changes in structure and cell cycle that are accompanied by altered expression and production of cytokines. These cytokines contribute to the initiation of the fibrotic response by favoring activation of fibroblasts, recruitment of inflammatory cells, and loss of endothelial cells. This review focuses on how augmented growth factor and cytokine production induces epithelial crosstalk with cells in the interstitium to promote progressive tubulointerstitial fibrosis after renal injury.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.