ArticleCell death & disease2023
GOLPH3 promotes endotoxemia-induced liver and kidney injury through Golgi stress-mediated apoptosis and inflammatory response.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- The role of Dymeclin in chronic unpredictable mild stress-induced depression: maintaining the Golgi apparatus structure and regulating NLRP3 inflammasome activation.Molecular medicine (Cambridge, Mass.) · 2026Article
- KLF2 alleviates sepsis-induced acute kidney injury via the lncRNA GAS6-AS2/GOLPH3 axis.BMC nephrology · 2026Article
- Spatiotemporal dynamics of reactive oxygen species: implications for cellular homeostasis and redox therapies.Cellular & molecular biology letters · 2026Review
- Regulated cell death in sepsis-associated liver injury: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Neutrophilic granule protein promotes lipopolysaccharide-induced iNOS/NO expression via JAK2/STAT1 signaling pathway and augments bacteria clearance of macrophages.Cellular and molecular life sciences : CMLS · 2025Article
- Constitutive Androstane Receptor in Macrophages Regulates Toll-Like Receptor 4-Mediated Innate Immune Responses Against Endotoxemic Liver Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cholesterol-driven pathological astrocytic responses in diabetes-associated cognitive impairment through astrocytic SCAP accumulation and NF-κB-C3 signaling modulation.Experimental & molecular medicine · 2025Article
- GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses.Scientific reports · 2025Article
- Sequential Targeting Chondroitin Sulfate-Bilirubin Nanomedicine Attenuates Osteoarthritis via Reprogramming Lipid Metabolism in M1 Macrophages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Bioinformatics study of the TNFRSF1A mechanism involved in acute liver injury in sepsis through the mTOR signaling pathway.Histology and histopathology · 2025Article
- GALNT3 in Ischemia-Reperfusion Injury of the Kidney.Journal of the American Society of Nephrology : JASN · 2025Article
- Transcriptional responses in different mouse models of septic liver injury differ from those in patients with septic liver injury.Frontiers in immunology · 2025Article
- Exploring the relationship between sepsis and Golgi apparatus dysfunction: bioinformatics insights and diagnostic marker discovery.Frontiers in genetics · 2025Article
- Interleukins-27 Aggravates Liver Injury by Impairing the Antimicrobial Response of Macrophages via the Promotion of Mitochondrial Dysfunction in the Context of Sepsis.Mediators of inflammation · 2025Article
- The identification of key molecules and pathways in the crosstalk of calcium oxalate-treated TCMK-1 cells and macrophage via exosomes.Scientific reports · 2024Article
- The Role of Interferon-Induced Proteins with Tetratricopeptide Repeats 1 and 2 in Sepsis-Induced Acute Liver Injury.Infection and drug resistance · 2024Article
- Screening of prognostic core genes based on cell-cell interaction in the peripheral blood of patients with sepsis.Open life sciences · 2024Article
- Galgravin Isolated fromInternational journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a serious clinical condition characterized by a systemic inflammatory response, a leading cause of acute liver and kidney injury, and is associated with a high morbidity and mortality. Understanding the molecular mechanisms underlying the acute liver and kidney injury is crucial for developing an effective therapy. Golgi apparatus plays important roles and has various substrates mediating cellular stress responses. Golgi phosphoprotein 3 (GOLPH3), linking Golgi membranes to the cytoskeleton, has been identified as an important oncogenic regulator; however, its role in endotoxemia-induced acute liver and kidney injury remains elusive. Here, we found that upregulation of GOLPH3 was associated with endotoxemia-induced acute liver and kidney injury. Lipopolysaccharide (LPS) treatment increased Golgi stress and fragmentation, and associated pro-inflammatory mediator (Tnfα, IL-6, and IL-1β) production in vivo and in vitro. Interestingly, the downregulation of GOLPH3 significantly decreased LPS-induced Golgi stress and pro-inflammatory mediators (Tnfα, IL-6, Mcp1, and Nos2), and reversed apoptotic cell deaths in LPS-treated hepatocytes and renal tubular cells. GOLPH3 knockdown also reduced inflammatory response in LPS-treated macrophages. The AKT/NF-kB signaling pathway was suppressed in GOLPH3 knockdown, which may be associated with a reduction of inflammatory response and apoptosis and the recovery of Golgi morphology and function. Taken together, GOLPH3 plays a crucial role in the development and progression of acute liver and kidney injury by promoting Golgi stress and increasing inflammatory response and apoptosis, suggesting GOLPH3 as a potential therapeutic target for endotoxemia-induced tissue injury.
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