ArticleCell death & disease2024
STING contributes to lipopolysaccharide-induced tubular cell inflammation and pyroptosis by activating endoplasmic reticulum stress in acute kidney injury.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 71 citations in OpenAlex.
- Microbial extracellular vesicles from min pigs remodel macrophage polarization via STING to sustain intestinal immune homeostasis.Gut microbes · 2026Article
- Discovery of a novel STING-binding peptide associated with reduced cGAMP-induced inflammatory gene expression.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- D4F-Functionalized Ceria Nanozyme-CasRx Platform Suppresses STING and Reprograms the Renal Immune Niche in Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PROTAC-mediated regulation of programmed cell death: From molecular mechanisms to therapeutic breakthroughs.Innovation (Cambridge (Mass.)) · 2026Review
- Mechanical ventilation activates PERK/eIF2α and NOD1 pathways that contribute to NF-κB-driven inflammation in VILI.Respiratory research · 2026Article
- Coenzyme Q10 protects against 6 GHz electromagnetic field-induced liver injury via suppression of inflammatory responses associated with NF-κB/p65 immunoreactivity and endoplasmic reticulum stress.Scientific reports · 2026Article
- uPAR/suPAR Signaling and Organ Crosstalk in Cardiovascular-Kidney-Metabolic Syndrome.Circulation research · 2026Review
- The Role and Therapeutic Potential of the STING Signaling Pathway in the Pathogenesis of Diabetic Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Mitochondria as convergence hubs for innate immunity pathways.Communications biology · 2026Review
- ESCRT-Mimetic Nanodegrader Targets STING for Anti-Inflammatory Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- STING is a key driver of Japanese encephalitis virus induced inflammatory response.Communications biology · 2026Article
- Research progress on biomarkers for acute kidney injury in children.Pediatric nephrology (Berlin, Germany) · 2026Review
- Pseudogene-Derived Long Noncoding RNAs GSTM3P1/Gstm2-ps1 Exacerbate Sepsis-Associated Acute Kidney Injury by Suppressing Their Parent Gene Translation.The American journal of pathology · 2026Article
- STING-STAT1-ZBP1 axis orchestrates PANoptotic signaling in ischemia-reperfusion induced acute kidney injury.Cell communication and signaling : CCS · 2026Article
- CXCR6+ T cells promote apoptosis and necroptosis in proximal tubules during AKI-to-CKD transition.Cell death & disease · 2026Article
- Triphenylphosphine bromide enhances the effect of nano-micellar drug delivery system loaded with ROS inhibitor TEMPO on acute lung injury.Journal of biological engineering · 2026Article
- Emerging Mechanistic Roles of STING Signaling in Kidney Diseases.The American journal of pathology · 2026Review
- PINK1 deacetylation by emodin-induced SIRT3 upregulation alleviates acute kidney injury by Inhibition of ferroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Recently, innate immunity and inflammation were recognized as the key factors for acute kidney injury (AKI) caused by sepsis, which is closely related to high mortality. Stimulator of interferon genes (STING) has emerged as a critical component of innate immune and inflammatory responses. However, the role of STING in the pathogenesis of septic AKI remains unclear. This study demonstrated that the STING was significantly activated in tubular cells induced by lipopolysaccharide (LPS) in vivo and in vitro. Tubule-specific STING knockout attenuated LPS-induced renal dysfunction and pathological changes. Mechanistically, the STING pathway promotes NOD-like receptor protein 3 (NLRP3) activation. STING triggers endoplasmic reticulum (ER) stress to induce mitochondrial reactive oxygen species (mtROS) overproduction, enhancing thioredoxin-interacting protein activation and association with NLRP3. Eventually, the NLRP3 inflammasome leads to tubular cell inflammation and pyroptosis. This study revealed the STING-regulated network and further identified the STING/ER stress/mtROS/NLRP3 inflammasome axis as an emerging pathway contributing to tubular damage in LPS-induced AKI. Hence, targeting STING may be a promising therapeutic strategy for preventing septic AKI.
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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.