ArticleCell proliferation2022
Triptolide promotes autophagy to inhibit mesangial cell proliferation in IgA nephropathy via the CARD9/p38 MAPK pathway.
Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Efficacy and safety of various immunosuppressive agents for pediatric Henoch-Schönlein purpura nephritis (IgA vasculitis nephritis) in Chinese children: a systematic review and network meta-analysis.Frontiers in immunology · 2026Pooled it
- Triptolide in renal disorders: dual roles of therapeutic potential and nephrotoxicity: a narrative review.Pharmaceutical biology · 2026Review
- NR1H4 downregulation facilitates abnormal cell proliferation contributing to IgA nephropathy pathogenesis, with potential clinical implications.Human cell · 2026Article
- Activatable nanoflytrap achieves synergistic "Capture-Block-Regulate" therapy of pancreatic ductal adenocarcinoma.Journal of nanobiotechnology · 2026Article
- Kidney Transcriptomic and Proteomic Analyses Provide New Insight into the Pathogenesis of IgA Nephropathy in Mice.Biochemical genetics · 2026Article
- Pleiotropic pharmacological activities and multiple-organ toxicities of triptolide: a programmed cell death perspective.Chinese medicine · 2026Review
- HE4: a potential diagnostic biomarker in autoimmune diseases.Central-European journal of immunology · 2026Review
- Kidney-targeted drug delivery: from physiological mechanisms to precision therapeutics.Frontiers in bioengineering and biotechnology · 2026Review
- Targeted modulation of intestinal barrier and mucosal immune-related microbiota attenuates IgA nephropathy progression.Gut microbes · 2025Article
- Glycine decarboxylase advances IgA nephropathy by boosting mesangial cell proliferation through the pyrimidine pathway.EMBO molecular medicine · 2025Article
- Targeting autophagy in autoimmune glomerular diseases.Journal of nephrology · 2025Review
- SOCS1 improves abnormal IgA galactosylation in IgA nephropathy by regulating the TLR9/MyD88 pathway.Immunologic research · 2025Article
- Hydroxychloroquine sulfate for IgA nephropathy: mechanisms and therapeutic potential in improving proteinuria and alleviating disease progression - a literature review.BMC nephrology · 2025Review
- HDAC9-mediated deacetylation of CALML6 promotes excessive proliferation of glomerular mesangial cells in IgA nephropathy.Clinical and experimental nephrology · 2025Article
- Exploring the Molecular Mechanism of Hydroxychloroquine Against IgAN Through Network Pharmacology, MD Simulations and Experimental Assessment.Journal of cellular and molecular medicine · 2025Article
- To establish and validate autophagy related biomarkers for the diagnosis of IgA nephropathy.Scientific reports · 2025Article
- EEPD1 regulates inflammation and endothelial apoptosis in atherosclerosis through KLF4-EEPD1-ERK axis.Clinical and translational medicine · 2025Article
- Single-Cell Analysis of Endothelial Cell Injury in IgA Nephropathy.Immunity, inflammation and disease · 2025Article
- Traditional Chinese medicine for HIV-related chronic comorbidities: evidence and potential therapeutic mechanisms.Frontiers in pharmacology · 2025Review
- Investigating the inflammatory mechanism of notoginsenoside R1 in Diabetic nephropathy via ITGB8 based on network pharmacology and experimental validation.Molecular medicine (Cambridge, Mass.) · 2024Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMesangial cell proliferation is the most basic pathological feature of immunoglobulin A nephropathy (IgAN); however, the specific underlying mechanism and an appropriate therapeutic strategy are yet to be unearthed. This study aimed to investigate the therapeutic effect of triptolide (TP) on IgAN and the mechanism by which TP regulates autophagy and proliferation of mesangial cells through the CARD9/p38 MAPK pathway.
methodsWe established a TP-treated IgAN mouse model and produced IgA1-induced human mesangial cells (HMC) and divided them into control, TP, IgAN, and IgAN+TP groups. The levels of mesangial cell proliferation (PCNA, cyclin D1, cell viability, and cell cycle) and autophagy (P62, LC3 II, and autophagy flux rate) were measured, with the autophagy inhibitor 3-Methyladenine used to explore the relationship between autophagy and proliferation. We observed CARD9 expression in renal biopsies from patients and analyzed its clinical significance. CARD9 siRNA and overexpression plasmids were constructed to investigate the changes in mesangial cell proliferation and autophagy as well as the expression of CARD9 and p-p38 MAPK/p38 MAPK following TP treatment.
resultsAdministering TP was safe and effectively alleviated mesangial cell proliferation in IgAN mice. Moreover, TP inhibited IgA1-induced HMC proliferation by promoting autophagy. The high expression of CARD9 in IgAN patients was positively correlated with the severity of HMC proliferation. CARD9/p38 MAPK was involved in the regulation of HMC autophagy and proliferation, and TP promoted autophagy to inhibit HMC proliferation by downregulating the CARD9/p38 MAPK pathway in IgAN.
conclusionTP promotes autophagy to inhibit mesangial cell proliferation in IgAN via the CARD9/p38 MAPK pathway.
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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 Socratic graph.