ArticleJournal of innate immunity2022
Porphyromonas gingivalis Gingipains-Mediated Degradation of Plasminogen Activator Inhibitor-1 Leads to Delayed Wound Healing Responses in Human Endothelial Cells.
Article in Journal of innate immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Gingipain inhibitors as an innovative therapy for periodontal and associated-systemic diseases: a systematic review.Clinical oral investigations · 2025Pooled it
- Article
- Effect of gut bacterial extracellular vesicles on angiogenic potential and vascular integrity: positive and negative aspects.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Exploring Matrix Stiffness-Related Gene in Periodontitis: A Comprehensive Multidataset Analysis.Mediators of inflammation · 2026Article
- Novel small molecule targeting PgQC reducesFrontiers in oral health · 2026Article
- Porphromonas gingivalis infection induces gingipain-dependent changes in the brain vasculature of zebrafish larvae.Cell communication and signaling : CCS · 2025Article
- Review
- Membrane vesicles from Red Complex bacteria: key players in oral pathogenesis, immune disruption, systemic diseases, and therapeutic insights.Frontiers in oral health · 2025Review
- Advances in the study of the relationship betweenFrontiers in cell and developmental biology · 2025Review
- Immunohistochemical Analysis to Evaluate the Efficacy of Tetracycline-Loaded Nano-Chitosan in Treating Periodontitis Induced byInternational journal of dentistry · 2025Article
- Oral Microbiome Dysbiosis as a Risk Factor for Stroke: A Comprehensive Review.Microorganisms · 2024Review
- MAT2A inhibition suppresses inflammation inJournal of oral microbiology · 2024Article
- Extracellular vesicles from periodontal pathogens regulate hepatic steatosis via Toll-like receptor 2 and plasminogen activator inhibitor-1.Journal of extracellular vesicles · 2024Article
- The Recruitment and Activation of Plasminogen by Bacteria-The Involvement in Chronic Infection Development.International journal of molecular sciences · 2023Review
- Review
- Extracts ofPharmaceutics · 2022Article
- Unexpected Relationships: Periodontal Diseases: Atherosclerosis-Plaque Destabilization? From the Teeth to a Coronary Event.Biology · 2022Review
- The impact of periodontitis on vascular endothelial dysfunction.Frontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasminogen activator inhibitor-1 (PAI-1), a serine protease inhibitor, is constitutively produced by endothelial cells and plays a vital role in maintaining vascular homeostasis. Chronic periodontitis is an inflammatory disease characterized by bleeding of periodontal tissues that support the tooth. In this study, we aimed to determine the role of PAI-1 produced by endothelial cells in response to infections caused by the primary periodontal pathogen Porphyromonas gingivalis. We demonstrated that P. gingivalis infection resulted in significantly reduced PAI-1 levels in human endothelial cells. This reduction in PAI-1 levels could be attributed to the proteolysis of PAI-1 by P. gingivalis proteinases, especially lysine-specific gingipain-K (Kgp). We demonstrated the roles of these degradative enzymes in the endothelial cells using a Kgp-specific inhibitor and P. gingivalis gingipain-null mutants, in which the lack of the proteinases resulted in the absence of PAI-1 degradation. The degradation of PAI-1 by P. gingivalis induced a delayed wound healing response in endothelial cell layers via the low-density lipoprotein receptor-related protein. Our results collectively suggested that the proteolysis of PAI-1 in endothelial cells by gingipains of P. gingivalis might lead to the deregulation of endothelial homeostasis, thereby contributing to the permeabilization and dysfunction of the vascular endothelial barrier.
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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 Socratic graph.