ArticleApplied biochemistry and biotechnology2022
Triptolide Alleviates Podocyte Epithelial-Mesenchymal Transition via Kindlin-2 and EMT-Related TGF-β/Smad Signaling Pathway in Diabetic Kidney Disease.
Article in Applied biochemistry and biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Comprehensive Evaluation of Triptolide's Therapeutic Mechanisms in Diabetic Kidney DiseaseCurrent pharmaceutical design · 2026Pooled it
- Natural products against renal fibrosis: molecular mechanisms, safety concerns, and translational perspectives.Renal failure · 2026Review
- Triptolide in renal disorders: dual roles of therapeutic potential and nephrotoxicity: a narrative review.Pharmaceutical biology · 2026Review
- TGF-β: elusive target in diabetic kidney disease.Renal failure · 2025Review
- Modified Huangqi Chifeng decoction alleviates podocyte injury on rat with experimental membranous nephropathy.Renal failure · 2025Article
- EIF4A3-induced circFAT1 promotes high glucose-induced podocyte damage via miR-30e-5p/SOX4 axis.RNA biology · 2025Article
- Targeted Delivery of Triptolide Alleviates Diabetic Nephropathy via Inactivation of JAK2-STAT1 Signaling.Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Traditional Chinese medicine for HIV-related chronic comorbidities: evidence and potential therapeutic mechanisms.Frontiers in pharmacology · 2025Review
- Kindlin-2 regulates the oncogenic activities of integrins and TGF-β in triple-negative breast cancer progression and metastasis.Oncogene · 2024Article
- Endothelial NOX5 Obliterates the Reno-Protective Effect of Nox4 Deletion by Promoting Renal Fibrosis via Activation of EMT and ROS-Sensitive Pathways in Diabetes.Antioxidants (Basel, Switzerland) · 2024Article
- Triptolide decreases podocytes permeability by regulating TET2-mediated hydroxymethylation of ZO-1.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Research Progress of Triptolide Against Fibrosis.Drug design, development and therapy · 2024Review
- Renalase protects against podocyte injury by inhibiting oxidative stress and apoptosis in diabetic nephropathy.Open life sciences · 2024Article
- Triptolide protects against podocyte injury in diabetic nephropathy by activating the Nrf2/HO-1 pathway and inhibiting the NLRP3 inflammasome pathway.Renal failure · 2023Article
- Btg2 Promotes Focal Segmental Glomerulosclerosis via Smad3-Dependent Podocyte-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Molecular Mechanistic Pathways Targeted by Natural Compounds in the Prevention and Treatment of Diabetic Kidney Disease.Molecules (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes-induced chronic kidney diseases are widespread and decrease the quality of life for millions of affected individuals in China. To date, no therapies effectively alleviate these conditions. Triptolide, a traditionally used Chinese medicine, has shown promise in treating renal diseases. Here, the study aimed to decipher the exact mechanism by which it functions. It was hypothesized that triptolide might prevent the epithelial-mesenchymal transition (EMT) of podocytes by activating the kindlin-2 and TGF-β/Smad pathways. Triptolide or telmisartan was intragastrically administered to 9-week-old db/db and dm/dm mice with diabetic nephropathy (DN) for 12 weeks. In addition, biochemical parameters and body weight were detected. WT-1, nephrin, podocin, E-cadherin, and α-SMA were determined by immunohistochemistry in the renal tissues of treated mice. Protein and mRNA expression of podocyte EMT markers, kindlin-2 and TGF-β/Smad, were analyzed to elucidate the underlying mechanism. It was observed that triptolide treatment relieved structural injuries and functional variations in diabetic mice. It also increased the protein and mRNA levels of nephrin, podocin, and E-cadherin and decreased the expression of α-SMA in diabetic mice. The protein and mRNA expressions of TGF-β1, p-SMAD3, and kindlin-2 decreased in diabetic kidneys following triptolide treatment. The findings demonstrated that triptolide might protect podocytes during DN by inhibiting podocyte EMT through inactivation of kindlin-2, combined with the downregulation of P-SMAD3 in the TGF-β/Smad signaling pathway.
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