ArticleKidney international2019
Renal tubular cell spliced X-box binding protein 1 (Xbp1s) has a unique role in sepsis-induced acute kidney injury and inflammation.
Article in Kidney international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 74 citations in OpenAlex.
- Metabolic-epigenetic rewiring of CCR5Science advances · 2026Article
- Caveolin-1 Stabilizes SERCA2 to Counteract Acute Kidney Injury via Suppression of CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation.Journal of advanced research · 2026Article
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- Xuebijing injection alleviates septic acute kidney injury by modulating inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress.Renal failure · 2025Article
- Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Review
- The Pathogenesis of Chronic Kidney Disease (CKD) and the Preventive and Therapeutic Effects of Natural Products.Current issues in molecular biology · 2025Review
- Renoprotective Effects of Phloretin and TUDCA via Simultaneous Inhibition of TLR4/MyD88/NF-κB and BiP/PERK/CHOP Pathways in AKI Under Diabetic Condition.Applied biochemistry and biotechnology · 2025Article
- Critical Role of S100A9 in Sepsis-associated Acute Kidney Injury: Mechanistic Insights through Pyroptosis Pathway Modulation.Inflammation · 2025Article
- The protective role of the IRE1α/XBP1 signaling cascade in autophagy during ischemic stress and acute kidney injury.Cell stress & chaperones · 2025Article
- Metabolomics- and proteomics-based multi-omics integration reveals early metabolite alterations in sepsis-associated acute kidney injury.BMC medicine · 2025Article
- Transcription factor XBP1s promotes endometritis-induced epithelial-mesenchymal transition by targeting MAP3K2, a key gene in the MAPK/ERK pathway.Cell communication and signaling : CCS · 2025Article
- CCL2 supports human hepatocytes long-term expansion for bioartificial liver therapy to relieve acute liver failure and extrahepatic complications.International journal of biological sciences · 2025Article
- Mechanisms and therapeutic prospects of hypoxia-inducible factor 1-alpha in acute kidney injury: a systematic review.Frontiers in cell and developmental biology · 2025Review
- High-mobility group box 1 in acute kidney injury.Frontiers in pharmacology · 2025Review
- 1, 6-dilauroyl-D-fructofuranose ameliorates lipopolysaccharide-induced septic acute kidney injury via inhibiting caspase 1 mediated pyroptosis formation in rat.Journal of the Chinese Medical Association : JCMA · 2024Article
- High-mobility group box 1 and its related receptors: potential therapeutic targets for contrast-induced acute kidney injury.International urology and nephrology · 2024Review
- STING contributes to lipopolysaccharide-induced tubular cell inflammation and pyroptosis by activating endoplasmic reticulum stress in acute kidney injury.Cell death & disease · 2024Article
- Acute kidney injury: exploring endoplasmic reticulum stress-mediated cell death.Frontiers in pharmacology · 2024Review
- Inhibition of BRD4 Attenuates ER Stress-induced Renal Ischemic-Reperfusion Injury.International journal of biological sciences · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
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Abstract
Sepsis is a systemic inflammatory state in response to infection, and concomitant acute kidney injury (AKI) increases mortality significantly. Endoplasmic reticulum stress is activated in many cell types upon microbial infection and modulates inflammation. The role of endoplasmic reticulum signaling in the kidney during septic AKI is unknown. Here we tested the role of the spliced X-box binding protein 1 (Xbp1s), a key component of the endoplasmic reticulum stress-activated pathways, in the renal response to sepsis in the lipopolysaccharide (LPS) model. Xbp1s was increased in the kidneys of mice treated with LPS but not in other models of AKI, or several chronic kidney disease models. The functional significance of Xbp1s induction was examined by genetic manipulation in renal tubules. Renal tubule-specific overexpression of Xbp1s caused severe tubule dilation and vacuolation with expression of the injury markers Kim1 and Ngal, the pro-inflammatory molecules interleukin-6 (Il6) and Toll-like receptor 4 (Tlr4), decreased kidney function and 50% mortality in five days. Renal tubule-specific genetic ablation of Xbp1 had no phenotype at baseline. However, after LPS, Xbp1 knockdown mice displayed lower renal NGAL, pro-apoptotic factor CHOP, serum creatinine levels, and a tendency towards lower Tlr4 compared to LPS-treated mice with intact Xbp1s. LPS treatment in Xbp1s-overexpressing mice caused a mild increase in NGAL and CHOP compared to LPS-treated mice without genetic Xbp1s overexpression. Thus, increased Xbp1s signaling in renal tubules is unique to sepsis-induced AKI and contributes to renal inflammation and injury. Inhibition of this pathway may be a potential portal to alleviate injury.
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