ArticleFrontiers in physiology2021
TRIM18-Regulated STAT3 Signaling Pathway
Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Ubiquitination-Related Diagnostic Biomarkers for Diabetic Nephropathy: Insights From Multiomic Analysis, Drug Docking, and Experimental Validation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Pro-inflammatory cytokine IFN-γ protects against renal fibrosis by promoting E3 ubiquitin ligase Trim21-mediated Loxl2 degradation in tubular epithelial cells.Cell death & disease · 2026Article
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- RNA-binding protein tristetraprolin inhibits Th2 cell activation and differentiation in allergic rhinitis by promoting TRIM18 mRNA decay.The Journal of biological chemistry · 2026Article
- Asprosin Aggravates Tubular Epithelial Cell Injury and Phenotypic Transformation via Mitochondrial Dynamics Disorder Mediated by Excessive Drp1 SUMOylation in Diabetic Nephropathy Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Ubiquitination in diabetes and its complications: A perspective from bibliometrics.World journal of diabetes · 2025Article
- A unique polygenic mouse model of obesity exhibits a distinct immunological profile that may offer protection against systemic inflammation, diabetes, and behavioral impairments.Frontiers in immunology · 2025Article
- Midline 1 associated with Fas signaling enhances murine antigen-induced arthritis.Frontiers in cell and developmental biology · 2025Article
- Midline-1 inhibited high glucose-induced epithelial-mesenchymal transition, fibrosis and inflammation through WNT/β-catenin signaling in benign prostatic hyperplasia.Frontiers in endocrinology · 2025Article
- WTAP-mediated mRedox report : communications in free radical research · 2024Article
- Erdr1 Drives Macrophage Programming via Dynamic Interplay with YAP1 and Mid1.ImmunoHorizons · 2024Article
- The E3 ubiquitin ligase TRIM39 modulates renal fibrosis induced by unilateral ureteral obstruction through regulating proteasomal degradation of PRDX3.Cell death discovery · 2024Article
- JAK/STAT3 signaling in cardiac fibrosis: a promising therapeutic target.Frontiers in pharmacology · 2024Review
- The effects of cGAS-STING inhibition in liver disease, kidney disease, and cellular senescence.Frontiers in immunology · 2024Review
- Erdr1 orchestrates macrophage polarization and determines cell fate via dynamic interplay with YAP1 and Mid1.bioRxiv : the preprint server for biology · 2023Article
- Article
- Capsaicin functions as a selective degrader of STAT3 to enhance host resistance to viral infection.Acta pharmacologica Sinica · 2023Article
- Folate Deficiency Enhanced Inflammation and Exacerbated Renal Fibrosis in High-Fat High-Fructose Diet-Fed Mice.Nutrients · 2023Article
- Sitagliptin Mitigates Diabetic Nephropathy in a Rat Model of Streptozotocin-Induced Type 2 Diabetes: Possible Role of PTP1B/JAK-STAT Pathway.International journal of molecular sciences · 2023Article
- HERC2 promotes inflammation-driven cancer stemness and immune evasion in hepatocellular carcinoma by activating STAT3 pathway.Journal of experimental & clinical cancer research : CR · 2023Article
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5 authors.
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Abstract
Diabetic kidney disease (DKD) has become a key cause of end-stage renal disease worldwide. Inflammation and fibrosis have been shown to play important roles in the pathogenesis of DKD. MID1, also known as TRIM18, is an E3 ubiquitin ligase of the tripartite motif (TRIM) subfamily of RING-containing proteins and increased in renal tubule in patients with DKD. However, the function and molecular mechanism of TRIM18 in DKD remain unexplored. Herein we report that TRIM18 expression levels were increased in patients with DKD. An animal study confirms that TRIM18 is involved in kidney injury and fibrosis in diabetic mice. TRIM18 knockdown inhibits high glucose (HG)-induced epithelial-mesenchymal transition (EMT), inflammation, and fibrosis of HK-2 cells. This is accompanied by decreased levels of tumor necrosis factor alpha, interleukin-6, hydroxyproline (Hyp), connective tissue growth factor, and α-smooth muscle actin. Additionally, TRIM18 knockdown inhibits HG-induced increase in the phosphorylated-/total signal transducer and activator of transcription (STAT3). Treatment with niclosamide (STAT3 inhibitor) or protein tyrosine phosphatase-1B (PTP1B) overexpression blocked the TRIM18 induced EMT, inflammation and fibrosis. Co-immunoprecipitation and Western blot assays showed that TRIM18 promoted the ubiquitination of PTP1B. These findings highlight the importance of the TRIM18/PTP1B/STAT3 signaling pathway in DKD and can help in the development of new therapeutics for DKD treatment.
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