ArticleFrontiers in immunology2018
Emerging Role of HMGB1 in the Pathogenesis of Schistosomiasis Liver Fibrosis.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Protective efficacy of dapagliflozin against schistosomiasis mansoni-induced liver pathology: an in vivo study.Scientific reports · 2026Article
- Mechanisms underlying persistent liver fibrosis progression in Schistosoma-infected individuals post-treatment.Infectious diseases of poverty · 2025Article
- The egg ribonuclease SjCP1412 accelerates liver fibrosis caused byParasitology · 2024Article
- Programmed cell death in hepatic fibrosis: current and perspectives.Cell death discovery · 2023Review
- A Miniature Biomedical Sensor for Rapid Detection ofBiosensors · 2023Article
- Interleukin-13 (IL-13)-A Pleiotropic Cytokine Involved in Wound Healing and Fibrosis.International journal of molecular sciences · 2023Review
- Diacerein ameliorates cholestasis-induced liver fibrosis in rat via modulating HMGB1/RAGE/NF-κB/JNK pathway and endoplasmic reticulum stress.Scientific reports · 2023Article
- High Mobility Group Box 1 (HMGB1): Potential Target in Sepsis-Associated Encephalopathy.Cells · 2023Review
- High mobility group box 1, ATP, lipid mediators, and tissue factor are elevated in COVID-19 patients: HMGB1 as a biomarker of worst prognosis.Clinical and translational science · 2023Article
- Deficiency of PKCλ/ι alleviates the liver pathologic impairment of Schistosoma japonicum infection by thwarting Th2 response.Parasites & vectors · 2022Article
- From Inflammation to Fibrosis: Novel Insights into the Roles of High Mobility Group Protein Box 1 in Schistosome-Induced Liver Damage.Pathogens (Basel, Switzerland) · 2022Review
- Effective delivery of osteopontin small interference RNA using exosomes suppresses liver fibrosisFrontiers in pharmacology · 2022Article
- The SIRT1-HMGB1 axis: Therapeutic potential to ameliorate inflammatory responses and tumor occurrence.Frontiers in cell and developmental biology · 2022Review
- Pathology and molecular mechanisms of Schistosoma japonicum-associated liver fibrosis.Frontiers in cellular and infection microbiology · 2022Review
- Hypoxia and the Receptor for Advanced Glycation End Products (RAGE) Signaling in Cancer.International journal of molecular sciences · 2021Review
- Epigenetic Markers Associated with Schistosomiasis.Helminthologia · 2021Article
- Article
- Serpinc1 Acts as a Tumor Suppressor in Hepatocellular Carcinoma Through Inducing Apoptosis and Blocking Macrophage Polarization in an Ubiquitin-Proteasome Manner.Frontiers in oncology · 2021Article
- RAGE Signaling in Melanoma Tumors.International journal of molecular sciences · 2020Review
- Necroptosis in Hepatosteatotic Ischaemia-Reperfusion Injury.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In chronic schistosomiasis, liver fibrosis is linked to portal hypertension, which is a condition associated with high mortality and morbidity. High mobility group box 1 (HMGB1) was originally described as a nuclear protein that functions as a structural co-factor in transcriptional regulation. However, HMGB1 can also be secreted into the extracellular milieu under appropriate signal stimulation. Extracellular HMGB1 acts as a multifunctional cytokine that contributes to infection, injury, inflammation, and immune responses by binding to specific cell-surface receptors. HMGB1 is involved in fibrotic diseases. From a clinical perspective, HMGB1 inhibition may represent a promising therapeutic approach for treating tissue fibrosis. In this study, we demonstrate elevated levels of HMGB1 in the sera in experimental mice or in patients with schistosomiasis. Using immunohistochemistry, we demonstrated that HMGB1 trafficking in the hepatocytes of mice suffering from acute schistosomiasis was inhibited by Glycyrrhizin, a well-known HMGB1 direct inhibitor, as well as by DIC, a novel and potential anti-HMGB1 compound. HMGB1 inhibition led to significant downregulation of IL-6, IL4, IL-5, IL-13, IL-17A, which are involved in the exacerbation of the immune response and liver fibrogenesis. Importantly, infected mice that were treated with DIC or GZR to inhibit HMGB1 pro-inflammatory activity showed a significant increase in survival and a reduction of over 50% in the area of liver fibrosis. Taken together, our findings indicate that HMGB1 is a key mediator of schistosomotic granuloma formation and liver fibrosis and may represent an outstanding target for the treatment of schistosomiasis.
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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.