ArticleMedical science monitor : international medical journal of experimental and clinical research2021
Gasdermin D Protects Mouse Podocytes Against High-Glucose-Induced Inflammation and Apoptosis via the C-Jun N-Terminal Kinase (JNK) Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 16 citations in OpenAlex.
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Targeting the NLRP3 inflammasome in kidney disease: molecular mechanisms, pathogenic roles, and emerging small-molecule therapeutics.Frontiers in immunology · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Identification of Senescence-Associated Biomarkers in Diabetic Glomerulopathy Using Integrated Bioinformatics Analysis.Journal of diabetes research · 2024Article
- Effects of Oltipraz on the Glycolipid Metabolism and the Nrf2/HO-1 Pathway in Type 2 Diabetic Mice.Drug design, development and therapy · 2024Article
- Lysophosphatidic Acid Induces Podocyte Pyroptosis in Diabetic Nephropathy by an Increase of Egr1 Expression via Downregulation of EzH2.International journal of molecular sciences · 2023Article
- Human Umbilical Cord Mesenchymal Stem Cells Inhibit Pyroptosis of Renal Tubular Epithelial Cells through miR-342-3p/Caspase1 Signaling Pathway in Diabetic Nephropathy.Stem cells international · 2023Article
- Process of Glucose Increases Rather Than Constant High Glucose Was the Main Cause of Abnormal Glucose Induced Glomerulus Epithelial Cells Inflammatory Response.International journal of molecular sciences · 2022Article
- Vitamin B6 Inhibits High Glucose-Induced Islet β Cell Apoptosis by Upregulating Autophagy.Metabolites · 2022Article
- PTEN-induced kinase 1 deficiency alters albumin permeability and insulin signaling in podocytes.Journal of molecular medicine (Berlin, Germany) · 2022Article
- HDAC11 promotes both NLRP3/caspase-1/GSDMD and caspase-3/GSDME pathways causing pyroptosis via ERG in vascular endothelial cells.Cell death discovery · 2022Article
- Cdc42 upregulation under high glucose induces podocyte apoptosis and impairs β-cell insulin secretion.Frontiers in endocrinology · 2022Article
- NLRP3-mediated pyroptosis in diabetic nephropathy.Frontiers in pharmacology · 2022Review
- Mini-Review: GSDME-Mediated Pyroptosis in Diabetic Nephropathy.Frontiers in pharmacology · 2021Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The inflammation and apoptosis of podocytes contribute to the pathological progression of diabetic nephropathy. Gasdermin D (GSDMD) plays an executive role in pyroptosis, but its effect on high-glucose (HG)-induced inflammation and apoptosis remains unclear. The aim of this study was to investigate the effect of GSDMD on high-glucose-induced inflammation and apoptosis in podocytes. MATERIAL AND METHODS Mouse podocytes were cultivated by high- or normal-glucose medium. We used western blot analysis, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and immunofluorescence to detect the expression and localization of GSDMD in high-glucose-induced podocytes, and the expression of apoptosis-related proteins Bax and Bcl-2, inflammatory factors IL-1ß, IL-6, and TNF-alpha, and JNK pathways in high-glucose-induced podocytes. Western blot and immunofluorescence were used to detect the expression and localization of synaptopodin under GSDMD knockdown and JNK-specific blocker SP600125. MitoSOX Red was used to detect the production of ROS in mitochondria under siGSDMD. The intracellular ROS generation was detected using a reactive oxygen species assay kit. RESULTS We found that GSDMD knockdown and JNK inhibition reduced the expression of Bax, Bcl-2, cleaved caspase-3, IL-1ß, IL-6, and TNF-alpha. Our results showed that GSDMD knockdown can inhibit HG-induced mitochondrial ROS production and JNK phosphorylation. CONCLUSIONS This study indicates that GSDMD knockdown can attenuate HG-induced inflammation and apoptosis by inhibiting the phosphorylation of JNK via mitochondrial ROS.
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