ArticleInternational journal of biological sciences2018
Triptolide Attenuates Renal Tubular Epithelial-mesenchymal Transition Via the MiR-188-5p-mediated PI3K/AKT Pathway in Diabetic Kidney Disease.
Article in International journal of biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses 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
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 113 citations in OpenAlex.
- Comprehensive Evaluation of Triptolide's Therapeutic Mechanisms in Diabetic Kidney DiseaseCurrent pharmaceutical design · 2026Pooled it
- The Role of MicroRNA in Contrast-Induced Nephropathy: A Scoping Review and Meta-Analysis.BioMed research international · 2020Pooled it
- Triptolide in renal disorders: dual roles of therapeutic potential and nephrotoxicity: a narrative review.Pharmaceutical biology · 2026Review
- Hyperglycemia in Diabetes Drives Hepatic Fibrosis Through the Non-Enzymatic Function of HK2 and AGEs-mediated Matrix Stiffening.International journal of biological sciences · 2026Article
- Tripterygium glycosides: recent advances in mechanisms, therapeutic applications, and safety optimization.Frontiers in medicine · 2026Review
- The PI3K-AKT-mTOR signaling pathway mediates epithelial mesenchymal transition and cytoskeletal architecture changes induce to renal fibrosis after Bisphenol S exposure.Scientific reports · 2025Article
- Immune cells mediate the effect of plasma lipidomes on IgA nephropathy: a Mendelian randomization study.Renal failure · 2025Article
- The Crosstalk with CXCL10-Rich Tumor-Associated Mast Cells Fuels Pancreatic Cancer Progression and Immune Escape.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unraveling the power of peptides fromNarra J · 2025Article
- Isorhamnetin attenuates renal interstitial fibrosis by targeting TWEAK/Fn14-mediated epithelial-mesenchymal transition.Frontiers in immunology · 2025Article
- The latest progression of N6-methyladenosine (mFrontiers in endocrinology · 2025Review
- Diabetic Kidney Disease: Disease Progression Driven by Positive Feedback Loops and Therapeutic Strategies Targeting Pathogenic Pathways.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy.Current molecular medicine · 2025Review
- Novel Insights into Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
- Effects of Phytochemicals on Type 2 Diabetes via MicroRNAs.Current nutrition reports · 2024Review
- The role of PI3K/Akt signaling pathway in chronic kidney disease.International urology and nephrology · 2024Review
- VDR restores the expression of PINK1 and BNIP3 in TECs of streptozotocin-induced diabetic mice.Life science alliance · 2024Article
- Crosstalk between MiRNAs/lncRNAs and PI3K/AKT signaling pathway in diabetes mellitus: Mechanistic and therapeutic perspectives.Non-coding RNA research · 2024Review
- Functions and targets of miRNAs in pharmacological and toxicological effects of major components of Tripterygium wilfordii Hook F.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Genetic imputation of kidney transcriptome, proteome and multi-omics illuminates new blood pressure and hypertension targets.Nature communications · 2024Article
8 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
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triptolide possesses the trait of renal protection. Epithelial-mesenchymal transition (EMT) is closely linked to the pathogenesis of diabetic kidney disease (DKD). MicroRNAs have recently emerged as critical regulators of DKD. However, it is poorly understood whether triptolide alleviates renal EMT by regulating microRNAs in DKD. In this study, we found that triptolide decreased albuminuria, improved the renal structure and reduced renal EMT in rats with DKD. Furthermore, activation of the PI3K/AKT signaling pathway was increased in diabetic rats, which was partly reversed by triptolide. Triptolide also alleviated glucose-induced EMT in HK-2 cells in vitro. PI3K/AKT signaling pathway activation was reduced after triptolide treatment. Moreover, triptolide decreased the increase in miR-188-5p expression stimulated by high glucose levels in HK-2 cells. miR-188-5p inhibited PTEN expression by directly interacting with the PTEN 3'-untranslated region. Additionally, downregulation of miR-188-5p, which imitates the effects of triptolide, attenuated the activation of the PI3K/AKT pathway and HG-induced EMT, whereas miR-188-5p overexpression reversed the effects of triptolide on the PI3K/AKT pathway and EMT. In conclusion, we demonstrated that triptolide ameliorates renal EMT via the PI3K/AKT signaling pathway through the interaction between miR-188-5p and PTEN, indicating that miR-188-5p may be a therapeutic target of triptolide in DKD.
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.