ArticleMediators of inflammation2019
RIPK2-Mediated Autophagy and Negatively Regulated ROS-NLRP3 Inflammasome Signaling in GMCs Stimulated with High Glucose.
Article in Mediators of inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- XIAP down-regulation inhibits RIPK2 ubiquitination-mediated insulin resistance.Endocrine connections · 2026Article
- Synergistic activity of simvastatin and irinotecan chemotherapy against glioblastoma converges on TGF-β signaling.Journal of neuro-oncology · 2025Article
- Targeting the NLRP3 inflammasome in kidney disease: molecular mechanisms, pathogenic roles, and emerging small-molecule therapeutics.Frontiers in immunology · 2025Review
- Pharmacological inhibition of receptor-interacting protein kinase 2 (RIPK2) elicits neuroprotective effects following experimental ischemic stroke.Experimental neurology · 2024Article
- HBx-induced PLARenal failure · 2023Article
- Paired protein kinases PRKCI-RIPK2 promote pancreatic cancer growth and metastasis via enhancing NF-κB/JNK/ERK phosphorylation.Molecular medicine (Cambridge, Mass.) · 2023Article
- Natural products in attenuating renal inflammationFrontiers in immunology · 2023Review
- High glucose represses the proliferation of tendon fibroblasts by inhibiting autophagy activation in tendon injury.Bioscience reports · 2022Article
- Analysis of Long Noncoding RNAs-Related Regulatory Mechanisms in Duchenne Muscular Dystrophy Using a Disease-Related lncRNA-mRNA Pathway Network.Genetics research · 2022Article
- Metabolic Dysfunction in the Regulation of the NLRP3 Inflammasome Activation: A Potential Target for Diabetic Nephropathy.Journal of diabetes research · 2022Review
- Article
- Silencing of PFKFB3 protects podocytes against high glucose‑induced injury by inducing autophagy.Molecular medicine reports · 2021Article
- lncRNA NEAT1 ameliorates LPS‑induced inflammation in MG63 cells by activating autophagy and suppressing the NLRP3 inflammasome.International journal of molecular medicine · 2021Article
- PCB118 Induces Inflammation of Islet Beta Cells via Activating ROS-NLRP3 Inflammasome Signaling.BioMed research international · 2021Article
- DsbA-L Ameliorates Renal Injury Through the AMPK/NLRP3 Inflammasome Signaling Pathway in Diabetic Nephropathy.Frontiers in physiology · 2021Article
- The Role of the Interplay Between Autophagy and NLRP3 Inflammasome in Metabolic Disorders.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHyperglycemia plays a vital role in diabetic nephropathy (DN); autophagy and its potential upregulator receptor-interacting protein kinase 2 (RIPK2) are associated with ROS, which play a potential role in regulating NLRP3, and may be involved in inflammation in DN.
aimIn this study, we aimed to explore the mechanisms mediated by RIPK2 in autophagy and the relationship with ROS-NLRP3 of DN, by investigating the levels of RIPK2 and autophagy in glomerular mesangial cells (GMCs) stimulated with high glucose. MATERIAL AND
methodsGMCs were divided into the following groups: normal group (NC), high glucose group (HG), and RIPK2 siRNA group. RIPK2, LC3, caspase1, and IL-1
resultsHigh glucose upregulated RIPK2 and LC3 in GMCs during short periods (0-12 h) (
conclusionsAutophagy was activated by high glucose at short time periods but was inhibited in the long term, demonstrating a dual role for high glucose in autophagy of GMCs. RIPK2 regulates ROS-NLRP3 inflammasome signaling through autophagy and may be involved in the pathogenesis of DN.
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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 OpenQuestion graph.