ArticleKidney international2025
The critical role of endoplasmic reticulum stress and the stimulator of interferon genes (STING) pathway in kidney fibrosis.
Article in Kidney international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Microbial extracellular vesicles from min pigs remodel macrophage polarization via STING to sustain intestinal immune homeostasis.Gut microbes · 2026Article
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- The Role of cGAS-STING-Driven PANoptosis in Neurodegenerative Diseases and Therapeutic Prospects.Cells · 2026Review
- Article
- Apical proximal tubule fatty acid uptake-generated ceramides cause endoplasmic reticulum stress from altered membrane fluidity.JCI insight · 2026Article
- Interferon-λ drives renal fibrosis by coordinating epithelial-fibroblast crosstalk.The Journal of experimental medicine · 2026Article
- EVA1A responds to endoplasmic reticulum stress to regulate renal fibrosis by promoting TGF-β signaling pathway.Journal of advanced research · 2026Article
- CaMaterials today. Bio · 2026Article
- Cyclosporine A promotes renal fibrosis through activating endoplasmic reticulum stress by targeting miR-212-5p/ATF6 axis.Journal of translational medicine · 2026Article
- STING-ERO1 signaling exacerbates PARylation-mediated parthanatos in sepsis.Cell communication and signaling : CCS · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Emerging Mechanistic Roles of STING Signaling in Kidney Diseases.The American journal of pathology · 2026Review
- Stimulator of Interferon Genes Is a Fine-Tuner, but Not a Prime Mover, of Kidney Inflammation.The American journal of pathology · 2026Article
- MUC20 alleviates kidney fibrosis by modulating pyroptosis through the MET/RAS/STING axis.Theranostics · 2026Article
- A stronger type I interferon signature distinguishes ANCA-associated vasculitis phenotypes and predicts kidney prognosis.Kidney international · 2026Article
- cGAS-STING pathway in innate immunity and its cell-specific role in kidney diseases.Frontiers in immunology · 2026Review
- HOXA2 exerts anti-renal fibrosis effects through reducing endoplasmic reticulum stress via the upregulation of SIRT1.Communications biology · 2025Article
- Intermodulation of endoplasmic reticulum stress and ferroptosis in diabetic nephropathy: molecular mechanisms and therapeutic potentials.Apoptosis : an international journal on programmed cell death · 2025Review
- Improved bioavailability and anti-nephrotoxicity efficacy of polydatin on cisplatin-induced AKIInternational journal of pharmaceutics: X · 2025Article
- [Elevated expressions of GRP78/CHOP in lupus nephritis: their diagnostic value and association with PERK/IRE1α pathway-mediated renal cell apoptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
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13 authors.
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Abstract
Endoplasmic reticulum (ER) stress is a condition in which the ER is overwhelmed and unable to manage its protein load properly. The precise activation mechanisms and role of ER stress in kidney disease remain unclear. To study this, we performed unbiased transcriptomics analysis to demonstrate ER stress in kidneys of patients with chronic kidney disease and in mouse models of acute and chronic kidney injury (cisplatin and unilateral ureteral obstruction and reanalyzed previously published data on folic acid and mitochondrial transcription factor A(TFAM) knockout mice). Inhibiting the protein kinase RNA-like ER kinase (PERK) arm of ER stress but not activating transcription factor 6 or inositol-requiring enzyme 1, protected mice from kidney fibrosis. The stimulator of interferon genes (STING) was identified as an important upstream activator of ER stress in kidney tubule cells. STING and PERK were found to physically interact, and STING agonists induced PERK activation in kidney tubule cells. Mice with a STING activating mutation presented with ER stress and kidney fibroinflammation. We also generated mice with a tubule specific STING deletion that were resistant to ER stress and kidney fibrosis. Human kidney spatial transcriptomics highlighted a spatial correlation between STING, ER stress and fibrotic gene expression. Thus, our results indicate that STING is an important upstream regulator of PERK and ER stress in tubule cells during kidney fibrosis development.
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