ArticleHypertension research : official journal of the Japanese Society of Hypertension2016
Toll-like receptor 4 signaling has a critical role in Porphyromonas gingivalis-accelerated neointimal formation after arterial injury in mice.
Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.
- Effects of Oral Inflammatory Diseases and Oral Hygiene on Atrial Fibrillation: A Systematic Review.International journal of clinical practice · 2023Pooled it
- TLR-4 Inhibition Attenuates Inflammation, Thrombosis, and Stenosis in Arteriovenous Fistula in Yucatan Miniswine.Cardiology and cardiovascular medicine · 2022Article
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Authors and funding
12 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Recently, we reported that a periodontopathic pathogen, Porphyromonas gingivalis (P. gingivalis), infection induced neointimal hyperplasia with enhanced expression of monocyte chemoattractant protein (MCP)-1 after arterial injury in wild-type mice. Toll-like receptor (TLR) 4 is known to be a key receptor for virulence factors of P. gingivalis. The aim of this study is to assess the hypothesis that TLR4 has a critical role in periodontopathic bacteria-induced neointimal formation after an arterial injury. Wild-type and TLR4-deficient mice were used in this study. The femoral arteries were injured, and P. gingivalis or vehicle was injected subcutaneously once per week. Fourteen days after arterial injury, murine femoral arteries were obtained for histopathological and immunohistochemical analyses. The anti-P. gingivalis IgG levels in P. gingivalis-infected groups were significantly increased compared with the anti-P. gingivalis IgG levels of the corresponding non-infected groups in both wild-type and TLR4-deficient mice. TLR4 deficiency negated P. gingivalis-induced neointimal formation compared with that observed in wild-type mice and reduced the number of MCP-1 positive cells in the neointimal area. We conclude that P. gingivalis infection may promote neointimal formation after an arterial injury through TLR4 signaling.
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