ArticleJournal of molecular and cellular cardiology2014
P. gingivalis lipopolysaccharide intensifies inflammation post-myocardial infarction through matrix metalloproteinase-9.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Guidelines for experimental models of myocardial ischemia and infarction.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Oral microbiota in cardiovascular health and disease.Frontiers in cellular and infection microbiology · 2025Review
- The heart-bone connection: relationships between myocardial infarction and osteoporotic fracture.American journal of physiology. Heart and circulatory physiology · 2024Review
- The multifaceted role of c-di-AMP signaling in the regulation ofFrontiers in cellular and infection microbiology · 2024Article
- Matrix metalloproteinases in coronary artery disease and myocardial infarction.Basic research in cardiology · 2023Review
- Framing Heartaches: The Cardiac ECM and the Effects of Age.International journal of molecular sciences · 2023Review
- Oral microbiome mediated inflammation, a potential inductor of vascular diseases: a comprehensive review.Frontiers in cardiovascular medicine · 2023Review
- Riding the wave: a quantitative report of electrocardiogram utilization for myocardial infarction confirmation.American journal of physiology. Heart and circulatory physiology · 2022Article
- Porphyromonas gingivalis outside the oral cavity.Odontology · 2022Review
- ChronicAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- Fibrosis after Myocardial Infarction: An Overview on Cellular Processes, Molecular Pathways, Clinical Evaluation and Prognostic Value.Medical sciences (Basel, Switzerland) · 2021Review
- Immune regulation of cardiac fibrosis post myocardial infarction.Cellular signalling · 2021Review
- Focusing Heart Failure Research on Myocardial Fibrosis to Prioritize Translation.Journal of cardiac failure · 2020Article
- Age- and sex-dependent differences in extracellular matrix metabolism associate with cardiac functional and structural changes.Journal of molecular and cellular cardiology · 2020Article
- Screening and Identification of Potential Hub Genes in Myocardial Infarction Through Bioinformatics Analysis.Clinical interventions in aging · 2020Article
- CD8American journal of physiology. Heart and circulatory physiology · 2019Article
- Identifying the molecular and cellular signature of cardiac dilation following myocardial infarction.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Fibroblast polarization over the myocardial infarction time continuum shifts roles from inflammation to angiogenesis.Basic research in cardiology · 2019Article
- Distal Consequences of Oral Inflammation.Frontiers in immunology · 2019Review
- The Mouse Heart Attack Research Tool 1.0 database.American journal of physiology. Heart and circulatory physiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Periodontal disease (PD) strongly correlates with increased mortality post-myocardial infarction (MI); however, the underlying mechanisms are unknown. Matrix metalloproteinase (MMP)-9 levels directly correlate with dysfunction and remodeling of the left ventricle (LV) post-MI. Post-MI, MMP-9 is produced by leukocytes and modulates inflammation. We have shown that exposure to Porphyromonas gingivalis lipopolysaccharide (PgLPS), an immunomodulatory molecule identified in PD patients, increases LV MMP-9 levels in mice and leads to cardiac inflammation and dysfunction. The aim of the study was to determine if circulating PgLPS exacerbates the LV inflammatory response post-MI through MMP-9 dependent mechanisms. We exposed wild type C57BL/6J and MMP-9(-/-) mice to PgLPS (ATCC 33277) for a period of 28 days before performing MI, and continued to deliver PgLPS for up to 7 days post-MI. We found systemic levels of PgLPS 1) increased MMP-9 levels in both plasma and infarcted LV resulting in reduced wall thickness and increased incidence of LV rupture post-MI and 2) increased systemic and local macrophage chemotaxis leading to accelerated M1 macrophage infiltration post-MI and decreased LV function. MMP-9 deletion played a protective role by attenuating the inflammation induced by systemic delivery of PgLPS. In conclusion, MMP-9 deletion has a cardioprotective role against PgLPS exposure, by attenuating macrophage mediated inflammation.
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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 OpenQuestion graph.