ArticleCell death & disease2015
Chop deficiency prevents UUO-induced renal fibrosis by attenuating fibrotic signals originated from Hmgb1/TLR4/NFκB/IL-1β signaling.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 104 citations in OpenAlex.
- Esaxerenone attenuates renal injury by inhibiting NR3C2-mediated inflammatory and fibrotic pathways.Renal failure · 2026Article
- Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- CanPharmaceuticals (Basel, Switzerland) · 2025Review
- Targeting JNK1/2 and P38 Mitogen-Activated Protein Kinases With Pazopanib Mitigates Bleomycin-Induced Lung Fibrosis.Archiv der Pharmazie · 2025Article
- Exploring mechanisms of radiation-induced myocardial fibrosis using HMGB1 neutralizing antibody.Journal of molecular histology · 2025Article
- Chop Deficiency Exacerbates Cyclophosphamide-Induced Overactive Bladder via Impaired Macrophage Apoptosis.Current medical science · 2025Article
- Direct fibroblast reprogramming: an emerging strategy for treating organic fibrosis.Journal of translational medicine · 2025Review
- High-mobility group box 1 in acute kidney injury.Frontiers in pharmacology · 2025Review
- A novel GCGR/GLP-1R dual-agonist TB001 ameliorates kidney fibrosis via inhibiting PERK-mediated endoplasmic reticulum stress pathway.Frontiers in immunology · 2025Article
- Protective Effects of Tormentic Acid on Unilateral Ureteral Obstruction-Induced Renal Injury, Inflammation, and Fibrosis: A Comprehensive Approach to Reducing Oxidative Stress, Apoptosis, and Ferroptosis.Antioxidants (Basel, Switzerland) · 2024Article
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- Endoplasmic Reticulum Stress-Mediated Cell Death in Renal Fibrosis.Biomolecules · 2024Review
- High-mobility group box 1 and its related receptors: potential therapeutic targets for contrast-induced acute kidney injury.International urology and nephrology · 2024Review
- Kangxianling formula attenuates renal fibrosis by regulating gut microbiota.European journal of medical research · 2024Article
- Protein-rich foods, sea foods, and gut microbiota amplify immune responses in chronic diseases and cancers - Targeting PERK as a novel therapeutic strategy for chronic inflammatory diseases, neurodegenerative disorders, and cancer.Pharmacology & therapeutics · 2024Review
- TXNIP aggravates cardiac fibrosis and dysfunction after myocardial infarction in mice by enhancing the TGFB1/Smad3 pathway and promoting NLRP3 inflammasome activation.Acta biochimica et biophysica Sinica · 2023Article
- Mannan-binding lectin ameliorates renal fibrosis by suppressing macrophage-to-myofibroblast transition.Heliyon · 2023Article
- Toll-like receptors 2 and 4 stress signaling and sodium-glucose cotransporter-2 in kidney disease.Molecular and cellular biochemistry · 2023Review
- Article
- MYBPC3 deficiency in cardiac fibroblasts drives their activation and contributes to fibrosis.Cell death & disease · 2022Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal fibrosis, particularly tubulointerstitial fibrosis is considered to be the final manifestation of almost all chronic kidney diseases (CKDs). Herein we demonstrated evidence that CHOP-related ER stress is associated with the development of renal fibrosis in both CKD patients and unilateral ureteral obstruction (UUO)-induced animals, and specifically, mice deficient in Chop were protected from UUO-induced renal fibrosis. Mechanistic studies revealed that loss of Chop protected tubular cells from UUO-induced apoptosis and secondary necrosis along with attenuated Hmgb1 passive release and active secretion. As a result, Chop deficiency suppressed Hmgb1/TLR4/NFκB signaling, which then repressed UUO-induced IL-1β production. Consequently, the IL-1β downstream Erk1/2 activity and its related c-Jun transcriptional activity were reduced, leading to attenuated production of TGF-β1 following UUO insult. It was further noted that reduced IL-1β production also inhibited UUO-induced PI3K/AKT signaling, and both of which ultimately protected mice from UUO-induced renal fibrosis. Together, our data support that suppression of CHOP expression could be a viable therapeutic strategy to prevent renal fibrosis in patients with CKDs.
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