ArticleScientific reports2017
p53 induces miR199a-3p to suppress SOCS7 for STAT3 activation and renal fibrosis in UUO.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 94 citations in OpenAlex.
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- Unveiling lactylation: A novel frontier in the pathogenesis of diabetic nephropathy (Review).International journal of molecular medicine · 2026Review
- Multi-omics analysis to identify the dynamic changes of immune cells and marker genes in renal fibrosis.Frontiers in genetics · 2026Article
- Exploring the molecular mechanism of budesonide enteric capsules in the treatment of IgA nephropathy based on bioinformatics.Scientific reports · 2025Article
- What a Modern Physician Should Know About microRNAs in the Diagnosis and Treatment of Diabetic Kidney Disease.International journal of molecular sciences · 2025Review
- PRDM16 acts as a homeostasis regulation factor to suppress the transition of AKI to CKD via upregulation of eukaryotic initiation factor 6.Cellular and molecular life sciences : CMLS · 2025Article
- miR-125b differentially impacts mineralization in dexamethasone and calcium-treated human mesenchymal stem cells.Molecular therapy. Nucleic acids · 2025Article
- Screening core genes for minimal change disease based on bioinformatics and machine learning approaches.International urology and nephrology · 2025Article
- Gastric cancer-derived exosomal let-7 g-5p mediated by SERPINE1 promotes macrophage M2 polarization and gastric cancer progression.Journal of experimental & clinical cancer research : CR · 2025Article
- Tamarix honey phenolics attenuate cisplatin-induced kidney toxicity by inhibition of inflammation mediated IL-6/STAT3/TNF-α and oxidative stress-dependent Nrf2/caspase-3 apoptotic signaling pathways.Frontiers in pharmacology · 2025Article
- Proregenerative MicroRNAs to Repair the Damaged Heart.European cardiology · 2025Review
- Circular RNAs in Organ Fibrosis.Advances in experimental medicine and biology · 2025Review
- Protective Effects of Tormentic Acid on Unilateral Ureteral Obstruction-Induced Renal Injury, Inflammation, and Fibrosis: A Comprehensive Approach to Reducing Oxidative Stress, Apoptosis, and Ferroptosis.Antioxidants (Basel, Switzerland) · 2024Article
- The crosstalk of Wnt/β-catenin signaling and p53 in acute kidney injury and chronic kidney disease.Kidney research and clinical practice · 2024Article
- Exosomal miR-199a-3p Secreted From Cancer-Associated Adipocytes Promotes Pancreatic Cancer Progression.Cancer medicine · 2024Article
- Alantolactone alleviates epithelial-mesenchymal transition by regulating the TGF-β/STAT3 signaling pathway in renal fibrosis.Heliyon · 2024Article
- The role of microRNA-142a in Toxoplasma gondii infection-induced downregulation of Foxp3: implications for adverse pregnancy outcomes.BMC infectious diseases · 2024Article
- Review
- Costunolide Inhibits Chronic Kidney Disease Development by Attenuating IKKβ/NF-κB Pathway.Drug design, development and therapy · 2024Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of p53 in renal fibrosis has recently been suggested, however, its function remains controversial and the underlying mechanism is unclear. Here, we show that pharmacological and genetic blockade of p53 attenuated renal interstitial fibrosis, apoptosis, and inflammation in mice with unilateral urethral obstruction (UUO). Interestingly, p53 blockade was associated with the suppression of miR-215-5p, miR-199a-5p&3p, and STAT3. In cultured human kidney tubular epithelial cells (HK-2), TGF-β1 treatment induced fibrotic changes, including collagen I and vimentin expression, being associated with p53 accumulation, p53 Ser15 phosphorylation, and miR-199a-3p expression. Inhibition of p53 by pifithrin-α blocked STAT3 activation and the expression of miR-199a-3p, collagen I, and vimentin during TGF-β1 treatment. Over-expression of miR-199a-3p increased TGFβ1-induced collagen I and vimentin expression and restored SOCS7 expression. Furthermore, SOCS7 was identified as a target gene of miR-199a-3p, and silencing of SOCS7 promoted STAT3 activation. ChIp analyses indicated the binding of p53 to the promoter region of miR-199a-3p. Consistently, kidney biopsies from patients with IgA nephropathy and diabetic nephropathy exhibited substantial activation of p53 and STAT3, decreased expression of SOCS7, and increase in profibrotic proteins and miR-199a-3p. Together, these results demonstrate the novel p53/miR-199a-3p/SOCS7/STAT3 pathway in renal interstitial fibrosis.
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