ArticleJournal of the American Society of Nephrology : JASN2016
Stat3 Controls Tubulointerstitial Communication during CKD.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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
60 citing papers in PubMed, 99 citations in OpenAlex.
- Retinoic Acid Receptor Responder Protein 1 Promotes Tubular Fibrosis via the KH RNA Binding Domain Containing, Signal Transduction Associated 1/Steroid Receptor Coactivator/p-Signal Transducer and Activator of Transcription 3 Axis.Journal of the American Society of Nephrology : JASN · 2026Article
- Downexpression of miR- 17 - 5p and miR- 125a- 5p is Potentially Associated with the Renal Impairment Through STAT- 3 and CD69 in Multiple Myeloma Adult Patients.Biochemical genetics · 2026Article
- Podocyte-Specific Deletion of STAT3 in Krüppel-Like Factor 4-Related Experimental Podocytopathy.Journal of the American Society of Nephrology : JASN · 2026Article
- PDIA3 Inhibition Facilitates Sensitivity of IKE-Induced Ferroptosis via STAT3/LCN2 Axis to Improve Glioblastoma Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Empagliflozin does not prevent progression of Dent's disease type 1 in a mouse model.Experimental physiology · 2026Article
- Biomarkers for Chronic Kidney Disease: An Updated Review of Innovative Detection Approaches.Current aging science · 2026Review
- Inflammation-Induced Klotho Deficiency: A Possible Key Driver of Chronic Kidney Disease Progression.International journal of general medicine · 2025Review
- Unveiling the material basis of Shenshuaifu granule and its therapeutic mechanism in chronic renal failure: a combined approach of high-resolution mass spectrometry andFrontiers in chemistry · 2025Article
- EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis.Experimental & molecular medicine · 2024Article
- Renal Epithelial Complement C3 Expression Affects Kidney Fibrosis Progression.International journal of molecular sciences · 2024Article
- STAT3 Protein-Protein Interaction Analysis Finds P300 as a Regulator of STAT3 and Histone 3 Lysine 27 Acetylation in Pericytes.Biomedicines · 2024Article
- Cardiotrophin-1 therapy reduces disease severity in a murine model of glomerular disease.Physiological reports · 2024Article
- STAT3 drives the expression of ACSL4 in acute kidney injury.iScience · 2024Article
- Protective Role of the Podocyte IL-15 / STAT5 Pathway in Focal Segmental Glomerulosclerosis.Kidney international reports · 2024Article
- The presence of xanthine dehydrogenase is crucial for the maturation of the rat kidneys.Clinical science (London, England : 1979) · 2024Article
- Higher density of CD4+ T cell infiltration predicts severe renal lesions and renal function decline in patients with diabetic nephropathy.Frontiers in immunology · 2024Article
- The Therapeutic Potential of CDK4/6 Inhibitors, Novel Cancer Drugs, in Kidney Diseases.International journal of molecular sciences · 2023Review
- [Therapeutic mechanism of Shenbing Decoction Ⅲ for renal fibrosis in chronic kidney disease: a study with network pharmacology, molecular docking and validation in rats].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- STAT-3 signaling role in an experimental model of nephropathy induced by doxorubicin.Molecular and cellular biochemistry · 2023Article
- Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023Review
Corrections and comments
- Commented on by
Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In CKD, tubular cells may be involved in the induction of interstitial fibrosis, which in turn, leads to loss of renal function. However, the molecular mechanisms that link tubular cells to the interstitial compartment are not clear. Activation of the Stat3 transcription factor has been reported in tubular cells after renal damage, and Stat3 has been implicated in CKD progression. Here, we combined an experimental model of nephron reduction in mice from different genetic backgrounds and genetically modified animals with in silico and in vitro experiments to determine whether the selective activation of Stat3 in tubular cells is involved in the development of interstitial fibrosis. Nephron reduction caused Stat3 phosphorylation in tubular cells of lesion-prone mice but not in resistant mice. Furthermore, specific deletion of Stat3 in tubular cells significantly reduced the extent of interstitial fibrosis, which correlated with reduced fibroblast proliferation and matrix synthesis, after nephron reduction. Mechanistically, in vitro tubular Stat3 activation triggered the expression of a specific subset of paracrine profibrotic factors, including Lcn2, Pdgfb, and Timp1. Together, our results provide a molecular link between tubular and interstitial cells during CKD progression and identify Stat3 as a central regulator of this link and a promising therapeutic target.
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.