ArticleLaboratory investigation; a journal of technical methods and pathology2018
High-mobility group box 1 induces endoplasmic reticulum stress and activates hepatic stellate cells.
Article in Laboratory investigation; a journal of technical methods and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Purinergic signaling in liver disease: calcium signaling and induction of inflammation.Purinergic signalling · 2025Review
- EZH2/miR-142-3p/HMGB1 axis mediates chondrocyte pyroptosis by regulating endoplasmic reticulum stress in knee osteoarthritis.Chinese medical journal · 2025Article
- Endoplasmic Reticulum-Targeting Natural Compounds: A Novel Frontier in Alleviating Liver Fibrosis.Drug design, development and therapy · 2025Review
- Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024Review
- Biomimetic mesenchymal stem cell membrane-coated nanoparticle delivery of MKP5 inhibits hepatic fibrosis through the IRE/XBP1 pathway.Journal of nanobiotechnology · 2024Article
- HMGB1 promotes mitochondrial transfer between hepatocellular carcinoma cells through RHOT1 and RAC1 under hypoxia.Cell death & disease · 2024Article
- Hepatic HRC induces hepatocyte pyroptosis and HSCs activation via NLRP3/caspase-1 pathway.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Article
- Auranofin prevents liver fibrosis by system Xc-mediated inhibition of NLRP3 inflammasome.Communications biology · 2021Article
- Reprogramming of microRNA expression via E2F1 downregulation promotes Salmonella infection both in infected and bystander cells.Nature communications · 2021Article
- 4-OI Attenuates Carbon Tetrachloride-Induced Hepatic Injury via Regulating Oxidative Stress and the Inflammatory Response.Frontiers in pharmacology · 2021Article
- Danger signals in liver injury and restoration of homeostasis.Journal of hepatology · 2020Review
- ER stress activates immunosuppressive network: implications for aging and Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2020Review
- The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis.BioMed research international · 2020Review
- Macrophage-derived HMGB1 is dispensable for tissue fibrogenesis.FASEB bioAdvances · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is a worldwide clinical issue. The activation of hepatic stellate cells (HSCs) is the central event during the hepatic fibrotic response. However, the exact mechanisms related to HSC activation and the connection between hepatocytes and HSCs remain unclear. We elucidated the mechanism by which the nuclear-damage-associated molecular pattern molecule, high-mobility group box 1 (HMGB1) was released from the impaired hepatocytes and induced endoplasmic reticulum stress to activate HSCs. In this work, we demonstrated that HMGB1 can be released from hepatocytes and the released HMGB1 activates the HSCs via ER stress at the transcriptional level which was dependent on the activation of both the TLR4 and RAGE signaling pathways rather than the TLR2 signaling pathway. HMGB1 induction of proinflammatory cytokines interleukin (IL)-1β and IL-18 release was dependent on ER stress. In vivo, stable inhibition of HMGB1 suppressed liver fibrosis. These results suggest that under damage condition, HMGB1 can be secreted from injured hepatocytes and activates TLR4- and RAGE signaling pathways to induce ER stress which activates HSCs. Moreover, HMGB1 can produce multiple inflammatory mediators through ER stress, which, in turn, promote liver fibrosis.
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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.