ArticleMolecular medicine reports2018
Spleen tyrosine kinase promotes NLR family pyrin domain containing 3 inflammasome‑mediated IL‑1β secretion via c‑Jun N‑terminal kinase activation and cell apoptosis during diabetic nephropathy.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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
23 citing papers in PubMed, 27 citations in OpenAlex.
- Sialyllactose Alleviates Streptozotocin-Induced Diabetes through Anti-Inflammatory and Metabolic Modulation.Biomolecules & therapeutics · 2025Article
- Regulation of pyroptosis in diabetic nephropathy by long non-coding and circular RNAs.Clinical and experimental medicine · 2025Review
- Unraveling diabetic kidney disease: insights from single-cell RNA sequencing.International urology and nephrology · 2025Review
- Targeting the NLRP3 inflammasome in kidney disease: molecular mechanisms, pathogenic roles, and emerging small-molecule therapeutics.Frontiers in immunology · 2025Review
- Role of the Innate Immune Response in Glomerular Disease Pathogenesis: Focus on Podocytes.Cells · 2024Review
- Research Progress of Pyroptosis in Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
- Single-Cell Sequencing Reveals the Expression of Immune-Related Genes in Macrophages of Diabetic Kidney Disease.Inflammation · 2024Article
- Mitochondrial P-JNK target, SAB (SH3BP5), in regulation of cell death.Frontiers in cell and developmental biology · 2024Review
- Identifying key genes for diabetic kidney disease by bioinformatics analysis.BMC nephrology · 2023Article
- GSDME-dependent pyroptosis signaling pathway in diabetic nephropathy.Cell death discovery · 2023Article
- Lacrimal Gland Epithelial Cells Shape Immune Responses through the Modulation of Inflammasomes and Lipid Metabolism.International journal of molecular sciences · 2023Article
- Natural products in attenuating renal inflammationFrontiers in immunology · 2023Review
- Novel insights into NOD-like receptors in renal diseases.Acta pharmacologica Sinica · 2022Review
- Metabolic Dysfunction in the Regulation of the NLRP3 Inflammasome Activation: A Potential Target for Diabetic Nephropathy.Journal of diabetes research · 2022Review
- Network Pharmacology Combined with Bioinformatics to Investigate the Mechanisms and Molecular Targets ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Role of Pyroptosis in Diabetes and Its Therapeutic Implications.Journal of inflammation research · 2021Review
- NEK7-Mediated Activation of NLRP3 Inflammasome Is Coordinated by Potassium Efflux/Syk/JNK Signaling DuringFrontiers in immunology · 2021Article
- New Insights into the Mechanisms of Pyroptosis and Implications for Diabetic Kidney Disease.International journal of molecular sciences · 2020Review
- The effect of spleen tyrosine kinase inhibitor R406 on diabetic retinopathy in experimental diabetic rats.International ophthalmology · 2020Article
- Identification of C3 as a therapeutic target for diabetic nephropathy by bioinformatics analysis.Scientific reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is a serious complication of diabetes and can cause an increased mortality risk. It was previously reported that NLR family pyrin domain containing 3 (NLRP3) inflammasome is involved in the pathogenesis of diabetes. However, the underlying mechanism is not clearly understood. In the present study, the effects of spleen tyrosine kinase (Syk) and c‑Jun N‑terminal kinase (JNK) on the NLRP3 inflammasome were examined in vivo and in vitro. Sprague‑Dawley rats were injected intraperitoneally with streptozotocin (65 mg/kg) to induce diabetes. HK2 cells and rat glomerular mesangial cells (RGMCs) were examined to detect the expression of JNK and NLRP3 inflammasome‑associated proteins following treatment with a Syk inhibitor or Syk‑small interfering (si)RNA in a high glucose condition. In the present study, it was revealed that the protein and mRNA expression levels of NLRP3 inflammasome‑associated molecules and the downstream mature interleukin (IL)‑1β were upregulated in vivo and in vitro. The Syk inhibitor and Syk‑siRNA suppressed high glucose‑induced JNK activation, and subsequently downregulated the activation of the NLRP3 inflammasome and mature IL‑1β in HK2 cells and RGMCs. Furthermore, high glucose‑induced apoptosis of HK2 cells was reduced by the Syk inhibitor BAY61‑3606. Therefore, the present results determined that high glucose‑induced activation of the NLRP3 inflammasome is mediated by Syk/JNK activation, which subsequently increased the protein expression level of IL‑1β and mature IL‑1β. The present study identified that the Syk/JNK/NLRP3 signaling pathway may serve a vital role in the pathogenesis of DN.
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.