ArticleScientific reports2020
Odontogenic infection by Porphyromonas gingivalis exacerbates fibrosis in NASH via hepatic stellate cell activation.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 69 citations in OpenAlex.
- Causal association between oral microbiota and hepatocellular carcinoma in East Asian populations: a Mendelian randomization study.Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Periodontitis aggravates high-fat diet-induced MASLD via gut microbiota dysbiosis and metabolic dysfunction in mice.Scientific reports · 2026Article
- Periodontitis and Chronic Liver Disease: Mechanistic Insights Focusing onMicroorganisms · 2026Review
- Ligature-induced periodontitis exacerbates high-carbohydrate/high-fat diet-induced fatty liver in mice under non-diabetic conditions.BMC oral health · 2026Article
- [Periodontitis and Metabolic Dysfunction-Associated Fatty Liver Disease: From Oral Dysbiosis to Hepatic Metabolic Dysregulation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Review
- Mechanisms underlying the role of the oral-gut-liver axis in the promotion of liver fibrosis by periodontal disease: an interacting network of inflammation, microbiota, and barrier function.Frontiers in cellular and infection microbiology · 2026Review
- Periodontitis and MASLD: a narrative review of the direct oral-hepatic pathway.Frontiers in cellular and infection microbiology · 2026Review
- Liver as a key organ for systemic antimicrobial defense.Hepatology communications · 2025Review
- Hepatic stellate cell inhibition by angiotensin II receptor blocker mitigates liver injury and fibrosis via NF-κB-galectin-3 suppression in a rat nonalcoholic steatohepatitis model.Archives of toxicology · 2025Article
- Interaction Between Periodontitis and MASLD: Pathophysiological Associations and Possibilities of Prevention and Therapy.Biomedicines · 2025Review
- Malocclusion Worsens Survival Following Sepsis Due to the Disruption of Innate and Acquired Immunity.International journal of molecular sciences · 2025Article
- The oral-gut microbiota axis: a link in cardiometabolic diseases.NPJ biofilms and microbiomes · 2025Review
- From gingiva to multiple organs in mice: The trace ofJournal of dental sciences · 2025Article
- Periodontal inflammation potentially inhibits hepatic cytochrome P450 expression and disrupts the omega-3 epoxidation pathway in a murine model.Journal of dental sciences · 2025Article
- Effect ofFEMS microbes · 2025Article
- Article
- Immunological dynamics in MASH: from landscape analysis to therapeutic intervention.Journal of gastroenterology · 2024Review
- Periodontitis promotes hepatocellular carcinoma in Stelic Animal model (STAM) mice.Scientific reports · 2024Article
- Interaction of periodontal clinical indicators in metabolic syndrome and nonalcoholic fatty liver disease: Implications for preventive interventions.The Saudi dental journal · 2024Article
- Multifunctional role of oral bacteria in the progression of non-alcoholic fatty liver disease.World journal of hepatology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Odontogenic infection of Porphyromonas gingivalis (P.g.), a major periodontal pathogen, exacerbates pathological progression of non-alcoholic steatohepatitis (NASH). In this study, we aimed to clarify the detailed mechanism in which P.g. induced hepatic stellate cells (HSCs; key effector cells in liver fibrosis) activation. In the liver of high fat diet-induced NASH mouse model with P.g. odontogenic infection, immunolocalization of P.g. was detected. The number of hepatic crown-like structure, which was macrophage aggregation and related to liver fibrosis, was drastically increased and fibrosis area was also increased through upregulating immunoexpression of Phosphorylated Smad2 (key signaling molecule of TGF-β1) and Galectin-3. P.g.-secreted trypsin-like enzyme [gingipain; an activator of protease-activated receptor 2 (PAR2)] stimulated HSC proliferation and differentiation through Smad and ERK signaling induced by TGF-β1 produced from HSCs with P.g.-infection. Further, Galectin-3 produced from HSCs with P.g. infection and P.g.-derived LPS/lipoprotein stimulation stabilized TGFβ-receptor II resulting in increasing sensitivity for TGF-β1, finally leading to HSC differentiation via activating Smad and ERK signaling. In addition to them, hepatocytes (main component cells of liver) contributed to HSC activation through TGF-β1 and Galectin-3 production in paracrine manner. Collectively, P.g.-odontogenic infection exacerbates fibrosis of NASH by HSC activation through TGF-β1 and Gal-3 production from HSCs and hepatocytes.
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