ArticleCell death & disease2023
Honokiol suppresses the aberrant interactions between renal resident macrophages and tubular epithelial cells in lupus nephritis through the NLRP3/IL-33/ST2 axis.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 30 citations in OpenAlex.
- Pharmacological advances of honokiol: Mechanisms, targets and therapeutic potential (Review).Biomedical reports · 2026Review
- Mitochondrial Regulation of the NLRP3 Inflammasome in Diabetic Kidney Disease: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2026Review
- The TRAF6-TXNIP-NLRP3 signaling axis regulates LPS-induced pyroptosis in glomerular podocytes.Journal of molecular histology · 2026Article
- Dual-mechanistic regulation of podocyte pyroptosis in lupus nephritis by the AP-1 complex: transcriptional activation of NLRP3 and lactate-mediated ubiquitination inhibition.Cell communication and signaling : CCS · 2026Article
- Identifying Crucial Genes Associated with Pyroptosis in Lupus Nephritis.Inflammation · 2026Article
- Knowledge Mapping of Macrophages in Renal Fibrosis: A Bibliometric Analysis from 2014 to 2025.Journal of inflammation research · 2026Review
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
- Structural dynamics, pathogenic mechanisms, and therapeutic targeting of the NLRP3 inflammasome in lupus nephritis.Frontiers in immunology · 2026Review
- Dual Phosphorylation of STAT1 at Y701/S727 by TNFα Drives AIM2-Mediated PANoptosis of Renal Tubular Epithelial Cells and Fibrotic Progression in Renal Allografts.International journal of biological sciences · 2026Article
- Mechanisms of NLRP3 inflammasome in chronic kidney disease and the effects of traditional Chinese medicines.Renal failure · 2025Review
- PPARG-centered regulatory network of ferroptosis in lupus nephritis: insights by integrated comprehensive bioinformatics analysis and machine learning.Clinical rheumatology · 2025Article
- Antibacterial, Photoprotective, Anti-Inflammatory, and Selected Anticancer Properties of Honokiol Extracted from Plants of the GenusInternational journal of molecular sciences · 2025Review
- A fluorescent STING ligand sensor for high-throughput screening of compounds that can enhance tumor immunotherapy.Cell reports methods · 2025Article
- Honokiol ameliorates pyroptosis in intestinal ischemia‑reperfusion injury by regulating the SIRT3‑mediated NLRP3 inflammasome.International journal of molecular medicine · 2025Article
- Spatial transcriptomics reveals regional characteristics of lupus nephritis in murine kidneys and immune response to prednisolone or Gancao Nourishing-Yin decoction therapies.Clinical and translational medicine · 2025Article
- Integrating network pharmacology, IPA, and molecular docking to reveal the anti-osteoporosis effects of EA and EB via the FAK pathway.Frontiers in pharmacology · 2025Article
- Tissue-resident macrophages and renal diseases: landscapes and treatment directions.Frontiers in immunology · 2025Review
- Sirt1 protects lupus nephritis by inhibiting the NLRP3 signaling pathway in human glomerular mesangial cells.Open life sciences · 2025Article
- Magnolol and honokiol: potential lead compounds for the new drug discovery in treating autoimmune diseases.Frontiers in pharmacology · 2025Article
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lupus nephritis (LN) is a type of immune-complex nephritis caused by systemic lupus erythematosus and is a major contributor to mortality and morbidity. Honokiol (HNK) has been found to have a therapeutic effect on LN, but its action mechanism remains unclear. In this study, we first demonstrated that HNK attenuates kidney injury in MRL/lpr mice. Results from RNA sequencing combined with ingenuity pathway analysis suggested that HNK plays an anti-LN role through inhibition of the NLRP3 inflammasome and IL33. GEO chip data, single-cell data, and clinical samples from LN patients demonstrated that the pyroptosis and IL-33/ST2 pathways are abnormally activated during the stage of LN. In vivo, similar to the results of the AAV-mediated NLRP3 shRNA MRL/lpr model, HNK downregulated serum and renal IL-33 levels, and suppressed NLRP3 inflammasome and the IL-33/ST2 axis in the kidney. In vitro, co-culturing NLRP3-overexpressing or IL-33 knocked-down rat renal macrophages with NRK-52E cells confirmed that NLRP3 activation in resident macrophages directly upregulates IL-33, which in turn mediates the IL-33/ST2/NF-κB pathway to promote the inflammatory response of renal tubular epithelial cells. Furthermore, a molecular docking model and surface plasmon resonance analysis were utilized to demonstrate a direct interaction between HNK and NLRP3. In conclusion, this study provides a novel anti-LN treatment strategy in which HNK plays a preventive and therapeutic role against LN by suppressing the abnormal crosstalk between renal resident macrophages and renal tubular epithelial cells by inhibiting the activation of the NLRP3/IL-33/ST2 axis.
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