ArticleInternational journal of biological sciences2017
Triptolide Suppresses Glomerular Mesangial Cell Proliferation in Diabetic Nephropathy Is Associated with Inhibition of PDK1/Akt/mTOR Pathway.
Article in International journal of biological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 60 citations in OpenAlex.
- Triptolide in renal disorders: dual roles of therapeutic potential and nephrotoxicity: a narrative review.Pharmaceutical biology · 2026Review
- METTL3/YTHDF3 mJournal of diabetes investigation · 2025Article
- CypA inhibits respiratory syncytial virus (RSV) replication by suppressing glycolysis through the downregulation of PKM2 expression.Journal of virology · 2025Article
- Tanshinone IIA suppresses the proliferation and fibrosis of mesangial cell in diabetic nephropathy though WTAP-mediated mScientific reports · 2025Article
- NLRP3 inflammasomes pathway: a key target for Metformin.Inflammopharmacology · 2025Review
- NLRP3 Inflammasome-Mediated Pyroptosis in Diabetic Nephropathy: Pathogenic Mechanisms and Therapeutic Targets.Journal of inflammation research · 2025Review
- 1.25(OH)2D3 decreases PCNA and mTOR expression and alleviates renal injury in Thy-1 nephritis rat model.PloS one · 2024Article
- Targeted drug delivery strategy: a bridge to the therapy of diabetic kidney disease.Drug delivery · 2023Article
- Triptolide protects against podocyte injury in diabetic nephropathy by activating the Nrf2/HO-1 pathway and inhibiting the NLRP3 inflammasome pathway.Renal failure · 2023Article
- Efficacy and safety of Tripterygium wilfordii multiglucoside for idiopathic membranous nephropathy: a systematic review with bayesian meta-analysis.Frontiers in pharmacology · 2023Article
- Molecular Mechanistic Pathways Targeted by Natural Compounds in the Prevention and Treatment of Diabetic Kidney Disease.Molecules (Basel, Switzerland) · 2022Review
- Coxsackievirus B3 infection induces glycolysis to facilitate viral replication.Frontiers in microbiology · 2022Article
- Influenza A Virus (H1N1) Infection Induces Glycolysis to Facilitate Viral Replication.Virologica Sinica · 2021Article
- TMEM116 is required for lung cancer cell motility and metastasis through PDK1 signaling pathway.Cell death & disease · 2021Article
- Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway.Molecular medicine reports · 2021Article
- LncRNA SOX2OT alleviates mesangial cell proliferation and fibrosis in diabetic nephropathy via Akt/mTOR-mediated autophagy.Molecular medicine (Cambridge, Mass.) · 2021Article
- Study of the Active Components and Molecular Mechanism ofFrontiers in molecular biosciences · 2021Article
- Triptolide: pharmacological spectrum, biosynthesis, chemical synthesis and derivatives.Theranostics · 2021Review
- The Efficacy of Triptolide in Preventing Diabetic Kidney Diseases: A Systematic Review and Meta-Analysis.Frontiers in pharmacology · 2021Review
- Long non-coding RNAExperimental and therapeutic medicine · 2020Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesangial cell proliferation has been identified as a mainly contributing factor to glomerulosclerosis, which is typical of diabetic nephropathy. However, the specific mechanisms and therapies remain unclear. PDK1 is a critical regulator of cell proliferation, but the specific role of PDK1 in diabetic nephropathy has not been fully illuminated. In the current study, we demonstrated that triptolide (TP) ameliorated albuminuria in the high fat diet/STZ-induced diabetic rats. TP also suppressed the increased proliferating cell markers Ki-67 and PCNA in the kidney tissues. Our results of MTT and cell cycle analysis further confirmed that TP significantly inhibited mesangial cell proliferation, and the inhibition of PDK1/Akt/mTOR pathway might be the underlying mechanisms. In addition, we also found that the PDK1 activator (PS48) could reverse the cell proliferation inhibition role of TP. These data suggest that TP may be useful in prevention of diabetic glomerulosclerosis and that PDK1/Akt/mTOR pathway might be the underlying mechanism.
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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.