ArticleCell death & disease2019
Inhibition of STAT3 in tubular epithelial cells prevents kidney fibrosis and nephropathy in STZ-induced diabetic mice.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 162 citations in OpenAlex.
- Metabolic surgery mitigates early kidney injury in obese youth with diabetes by suppressing mTORC1/JAK/STAT signaling.The Journal of clinical investigation · 2026Trial
- The deubiquitinase YOD1 in renal tubular epithelial cells promotes diabetic kidney disease by stabilizing KEAP1.Acta pharmacologica Sinica · 2026Article
- Pathology-Anchored Biomarker Research Progress for the Early Diagnosis of Diabetic Kidney Disease: From Pathological Association to Early Validation.Biomedicines · 2026Review
- AI-Integrated Multi-Target Validation ofFoods (Basel, Switzerland) · 2026Article
- APLNR reduction in kidney-muscle crosstalk in renal model recovered by exercise and STAT3 inhibition.Biochemistry and biophysics reports · 2026Article
- Induction of fibrosis in human kidney organoids delineates mechanisms and therapeutic targets of fibrotic kidney disease.Stem cell research & therapy · 2026Article
- A Protective Role of Hydrogen Sulfide Donor GYY4137 Through Activated Microglia-induced Anti-inflammatory Cytokines in the Spinal Cord of Diabetic Rats.Molecular neurobiology · 2026Article
- Mechanism ofRenal failure · 2025Article
- Comprehensive analysis of pyroptosis-related gene signatures in renal fibrosis.Clinical and experimental nephrology · 2025Article
- Association of fructose-1,6-diphosphatase 1 with the progression of diabetic kidney disease.Nutrition & metabolism · 2025Article
- SETD7 exacerbates diabetic nephropathy through activating ACell & bioscience · 2025Article
- Multi-Omics Alterations in Rat Kidneys upon Chronic Glyphosate Exposure.Biomolecules · 2025Article
- Complement pathway: Risk molecular pattern of cardiovascular diseases in patients with diabetic nephropathy.Journal of medical biochemistry · 2025Article
- Isoquercitrin Alleviates Diabetic Nephropathy by Inhibiting STAT3 Phosphorylation and Dimerization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Administration of Purified Alpha-1 Antitrypsin in Salt-Loaded Hypertensive 129Sv Mice Attenuates the Expression of Inflammatory Associated Proteins in the Kidney.Biomolecules · 2025Article
- Decoding diabetic kidney disease: a comprehensive review of interconnected pathways, molecular mediators, and therapeutic insights.Diabetology & metabolic syndrome · 2025Review
- Elevation of ISG15 promotes diabetic kidney disease by modulating renal tubular epithelial cell pyroptosis.Clinical and translational medicine · 2025Article
- Effect of miR-29a-3p on renal interstitial fibrosis in diabetic kidney disease through FOXP1-mediated TGF-β1/Smad3 signaling pathway.Cytotechnology · 2025Article
- SP1 activates AKT3 to facilitate the development of diabetic nephropathy.Journal of endocrinological investigation · 2025Article
- Comprehending the Role of Metabolic and Hemodynamic Factors Alongside Different Signaling Pathways in the Pathogenesis of Diabetic Nephropathy.International journal of molecular sciences · 2025Review
29 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidences indicate that signal transducer and activator of transcription 3 (STAT3) is one of the crucial signaling pathways in the progression of diabetic nephropathy (DN). Here, we investigated the hypothesis that pharmacological blockade of STAT3 limits the progression of DN. Treatment with selective STAT3 inhibitor, S3I-201 for 16 weeks significantly attenuated kidney injuries in streptozotocin (STZ) induced diabetic mice, associated with downregulated expression of TGF-β1, ACE/AT1, and VEGF in diabetic mouse kidneys. Similar results were confirmed using genetic knockdown of STAT3 in mouse kidneys by injections of AAV2 expressing STAT3 shRNA in diabetic mouse. Further, STAT3 localization in kidney tissue was evaluated using immunofluorescent double-staining analysis, which indicated that STAT3 expression was mainly in the tubular epithelial cells. As expected, in renal tubular epithelial NRK-52E cells, high glucose (HG)-induced overexpression of TGF-β1, ACE/AT1, and VEGF were abrogated by S3I-201 pretreatment, as well as by genetic knockdown of STAT3 using specific siRNA sequence. This study found that renal tubular epithelial cells contributed to STAT3-mediated progression of DN and provided the first evidence that pharmacological inhibition of STAT3 attenuates DN.
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