ReviewFrontiers in medicine2020
Pro- and Anti-fibrogenic Functions of Gram-Negative Bacterial Lipopolysaccharide in the Liver.
Review in Frontiers in medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Clinical and immunological comparison of COVID-19 disease between critical and non-critical courses: a systematic review and meta-analysis.Frontiers in immunology · 2024Pooled it
- Gut microbiota and macrophage crosstalk: implications for colitis-associated colorectal cancer.Frontiers in cellular and infection microbiology · 2026Review
- Gut Microbiota Changes in Metabolic Dysfunction-Associated Steatohepatitis and Inflammatory Bowel Disease: Common Pathogenic Features.Current issues in molecular biology · 2025Review
- Exploring the impact of sleep duration and sleep disorders on metabolic dysfunction-associated steatotic liver disease in older adults.BMC geriatrics · 2025Article
- Liver injury in sepsis: manifestations, mechanisms and emerging therapeutic strategies.Frontiers in immunology · 2025Review
- Proanthocyanidins-Based Synbiotics as a Novel Strategy for Nonalcoholic Fatty Liver Disease (NAFLD) Risk Reduction.Molecules (Basel, Switzerland) · 2024Review
- Melissa officinalis extract palliates redox imbalance and inflammation associated with hyperthyroidism-induced liver damage by regulating Nrf-2/ Keap-1 gene expression in γ-irradiated rats.BMC complementary medicine and therapies · 2024Article
- The role of macrophages in liver fibrosis: composition, heterogeneity, and therapeutic strategies.Frontiers in immunology · 2024Review
- Citral-Enriched Fraction of Lemon Essential Oil Mitigates LPS-Induced Hepatocyte Injuries.Biology · 2023Article
- Evogliptin Directly Inhibits Inflammatory and Fibrotic Signaling in Isolated Liver Cells.International journal of molecular sciences · 2022Article
- Feedback loop between hepatocyte nuclear factor 1α and endoplasmic reticulum stress mitigates liver injury by downregulating hepatocyte apoptosis.Scientific reports · 2022Article
- Translational Approaches with Antioxidant Phytochemicals against Alcohol-Mediated Oxidative Stress, Gut Dysbiosis, Intestinal Barrier Dysfunction, and Fatty Liver Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Transcriptional Profiling of Porcine HCC Xenografts Provides Insights Into Tumor Cell Microenvironment Signaling.Frontiers in genetics · 2021Article
- Polarization of Macrophages in Insects: Opening Gates for Immuno-Metabolic Research.Frontiers in cell and developmental biology · 2021Review
- Article
- TLR4 Deficiency Exacerbates Biliary Injuries and Peribiliary Fibrosis Caused byFrontiers in cellular and infection microbiology · 2020Article
- Restricted intake of sulfur-containing amino acids reversed the hepatic injury induced by excessGut microbesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Extensive research performed over several decades has identified cells participating in the initiation and progression of fibrosis, and the numerous underlying inter- and intra-cellular signaling pathways. However, liver fibrosis continues to be a major clinical challenge as the precise targets of treatment are still elusive. Activation of physiologically quiescent perisinusoidal hepatic stellate cells (HSCs) to a myofibroblastic proliferating, contractile and fibrogenic phenotype is a critical event in the pathogenesis of chronic liver disease. Thus, elucidation of the mechanisms of the reversal to quiescence or inhibition of activated HSCs, and/or their elimination via apoptosis has been the focus of intense investigation. Lipopolysaccharide (LPS), a gut-resident Gram-negative bacterial endotoxin, is a powerful pro-inflammatory molecule implicated in hepatic injury, inflammation and fibrosis. In both acute and chronic liver injury, portal venous levels of LPS are elevated due to increased intestinal permeability. LPS, via CD14 and Toll-like receptor 4 (TLR4) and its adapter molecules, stimulates macrophages, neutrophils and several other cell types to produce inflammatory mediators as well as factors that can activate HSCs and stimulate their fibrogenic activity. LPS also stimulates synthesis of pro- and anti-inflammatory cytokines/chemokines, growth mediators and molecules of immune regulation by HSCs. However, LPS was found to arrest proliferation of activated HSCs and to convert them into non-fibrogenic phenotype. Interestingly, LPS can elicit responses in HSCs independent of CD14 and TLR4. Identifying and/or developing non-inflammatory but anti-fibrogenic mimetics of LPS could be relevant for treating liver fibrosis.
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What OpenQuestion holds
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.