ArticleMediators of inflammation2013
Toll-like receptor 9 promotes cardiac inflammation and heart failure during polymicrobial sepsis.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Modulation of inflammasome components in patients with heart failure using oral nutritional supplements: investigating the molecular mechanisms beyond the clinical benefit.European journal of nutrition · 2026Trial
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Article
- Anti-Inflammatory and Proliferative Properties of Luteolin-7-O-Glucoside.International journal of molecular sciences · 2021Article
- NETosis as a Pathogenic Factor for Heart Failure.Oxidative medicine and cellular longevity · 2021Review
- Complement as a Major Inducer of Harmful Events in Infectious Sepsis.Shock (Augusta, Ga.) · 2020Review
- The peripheral blood transcriptome in septic cardiomyopathy: an observational, pilot study.Intensive care medicine experimental · 2019Article
- Antioxidant and Cardioprotective Effects of EPA on Early Low-Severity Sepsis through UCP3 and SIRT3 Upholding of the Mitochondrial Redox Potential.Oxidative medicine and cellular longevity · 2019Article
- Triaryl Pyrazole Toll-Like Receptor Signaling Inhibitors: Structure-Activity Relationships Governing Pan- and Selective Signaling Inhibitors.ChemMedChem · 2018Article
- Harmful Roles of TLR3 and TLR9 in Cardiac Dysfunction Developing during Polymicrobial Sepsis.BioMed research international · 2018Article
- The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure.Mediators of inflammation · 2018Review
- Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status.Physiological reports · 2017Article
- [Heart in sepsis : Molecular mechanisms, diagnosis and therapy of septic cardiomyopathy].Der Anaesthesist · 2017Review
- Global TLR2 and 4 deficiency in mice impacts bone resorption, inflammatory markers and atherosclerosis to polymicrobial infection.Molecular oral microbiology · 2017Article
- Heart-resident CCR2JCI insight · 2016Article
- Microbial Nucleic Acid Sensing in Oral and Systemic Diseases.Journal of dental research · 2016Review
- Inhibition of Toll-like receptor 9 attenuates sepsis-induced mortality through suppressing excessive inflammatory response.Cellular immunology · 2015Article
- Mitochondrial ROS Induces Cardiac Inflammation via a Pathway through mtDNA Damage in a Pneumonia-Related Sepsis Model.PloS one · 2015Article
- Interleukin 6 increases dysfunction of organs in sepsis rats through sirtuin 1.International journal of clinical and experimental medicine · 2014Article
- Epigenetics, inflammation and metabolism in right heart failure associated with pulmonary hypertension.Pulmonary circulationArticle
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAim was to elucidate the role of toll-like receptor 9 (TLR9) in cardiac inflammation and septic heart failure in a murine model of polymicrobial sepsis.
methodsSepsis was induced via colon ascendens stent peritonitis (CASP) in C57BL/6 wild-type (WT) and TLR9-deficient (TLR9-D) mice. Bacterial load in the peritoneal cavity and cardiac expression of inflammatory mediators were determined at 6, 12, 18, 24, and 36 h. Eighteen hours after CASP cardiac function was monitored in vivo. Sarcomere length of isolated cardiomyocytes was measured at 0.5 to 10 Hz after incubation with heat-inactivated bacteria.
resultsCASP led to continuous release of bacteria into the peritoneal cavity, an increase of cytokines, and differential regulation of receptors of innate immunity in the heart. Eighteen hours after CASP WT mice developed septic heart failure characterised by reduction of end-systolic pressure, stroke volume, cardiac output, and parameters of contractility. This coincided with reduced cardiomyocyte sarcomere shortening. TLR9 deficiency resulted in significant reduction of cardiac inflammation and a sustained heart function. This was consistent with reduced mortality in TLR9-D compared to WT mice.
conclusionsIn polymicrobial sepsis TLR9 signalling is pivotal to cardiac inflammation and septic heart failure.
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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.