ArticleWorld journal of gastroenterology2020
Hepatic microenvironment underlies fibrosis in chronic hepatitis B patients.
Article in World journal of gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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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
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.
- The efficacy of traditional Chinese medicine on immune function in patients with hepatitis B-related liver fibrosis or cirrhosis: a systematic review and meta-analysis.Frontiers in medicine · 2026Pooled it
- Candidate gene polymorphisms associated with silicosis and coal workers' pneumoconiosis: a systematic review and meta-analysis.BMC pulmonary medicine · 2024Pooled it
- AURKA regulates HBV-induced hepatic stellate cell inflammation and liver fibrosis by modulating K48-linked ubiquitination and proteasomal degradation of TLR3.Journal of bioenergetics and biomembranes · 2026Article
- Discriminative Role of Interleukin-6, Neuropilin-1, and Amphiregulin for Cirrhosis in Patients with Chronic Hepatitis B Infection.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026Article
- Alterations in macular microvasculature in chronic hepatitis B patients measured by optical coherence tomography angiography.Quantitative imaging in medicine and surgery · 2026Article
- RAB25 promotes hepatitis B virus-induced liver fibrosis progression through activation of the PI3K/AKT signaling pathway.Virus research · 2026Article
- Advances in the understanding of the role and mechanism of action of PFKFB3‑mediated glycolysis in liver fibrosis (Review).International journal of molecular medicine · 2024Review
- Review of the Effects of Antiviral Therapy on Hepatitis B/C-Related Mortality and the Regression of Fibrosis.Viruses · 2024Review
- HIV coinfection exacerbates HBV-induced liver fibrogenesis through a HIF-1α- and TGF-β1-dependent pathway.Journal of hepatology · 2024Article
- Nanogene editing drug delivery systems in the treatment of liver fibrosis.Frontiers in medicine · 2024Review
- Development of Therapy Based on the Exploration of Biological Events Underlying the Pathogenetic Mechanisms of Chronic Hepatitis B Infection.Biomedicines · 2023Review
- Mesenchymal stem cells reversibly de-differentiate myofibroblasts to fibroblast-like cells by inhibiting the TGF-β-SMAD2/3 pathway.Molecular medicine (Cambridge, Mass.) · 2023Article
- Insights into the impact of hepatitis B virus on hepatic stellate cell activation.Cell communication and signaling : CCS · 2023Review
- RDW-SD is Superior to RDW-CV in Reflecting Liver Fibrosis Stage in Patients with Chronic Hepatitis B.Infection and drug resistance · 2023Article
- Correlation of Serum M-CSF, CER, and TIMP-1 Levels with Liver Fibrosis in Viral Hepatitis.Computational and mathematical methods in medicine · 2022Article
- Hepatocellular Carcinoma Tumor Microenvironment and Its Implications in Terms of Anti-tumor Immunity: Future Perspectives for New Therapeutics.Journal of gastrointestinal cancer · 2021Review
- Anti-Hepatocellular Carcinoma Effect and Molecular Mechanism of the Estrogen Signaling Pathway.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic hepatitis B virus (HBV) infection is a leading cause of liver morbidity and mortality worldwide. Liver fibrosis resulting from viral infection-associated inflammation and direct liver damage plays an important role in disease management and prognostication. The mechanisms underlying the contribution of the liver microenvironment to fibrosis in HBV patients are not fully understood. There is an absence of effective clinical treatments for liver fibrosis progression; thus, establishing a suitable
aimTo examine a subset of pre-selected microenvironment factors of chronic HBV patients that may underlie fibrosis, with a focus on fibroblast activation.
methodsWe examined the gene expression of key microenvironment factors in liver samples from patients with more advanced fibrosis compared with those with less severe fibrosis. We also used the human stellate cell line LX-2 in the
resultsOf the secreted factors examined, transforming growth factor (TGF)-β1, interleukin (IL)-1β and tumor necrosis factor (TNF)-α were increased in patients with advanced fibrosis. We found that besides TGF-β1, IL-1β can also induce a profibrotic cascade by stimulating the expression of connective tissue growth factor and platelet-derived growth factor (PDGF) in LX-2 cells. Furthermore, the proinflammatory response can be elicited in LX-2 cells following treatment with IL-1β and TNF-α, suggesting that stellate cells can respond to proinflammatory stimuli. By combining IL-1β and TGF-β1, we observed not only fibroblast activation as shown by αlpha-smooth muscle actin and PDGF induction, but also the inflammatory response as shown by increased expression of IL-1β.
conclusionCollectively, our data from HBV patients and
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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.