ArticleThe Journal of biological chemistry2015
Cardiac RNA induces inflammatory responses in cardiomyocytes and immune cells via Toll-like receptor 7 signaling.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
39 citing papers in PubMed, 61 citations in OpenAlex.
- Toll-like receptor 7 constrains efferocytosis in myocardial injury.Basic research in cardiology · 2026Article
- TLR7 inhibition limits cardiac ischemic injury by disrupting ITGAM-dependent immune-endothelial interaction.bioRxiv : the preprint server for biology · 2026Article
- Article
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Immunization induces inflammation in the mouse heart during spaceflight.BMC genomics · 2025Article
- Technological breakthroughs and advancements in the application of mRNA vaccines: a comprehensive exploration and future prospects.Frontiers in immunology · 2025Review
- From stress signals to fertility challenges: the role of damage-associated molecular patterns in male reproduction.Frontiers in immunology · 2025Review
- Protective effect and mechanism of Qingfei Paidu decoction on myocardial damage mediated by influenza viruses.Frontiers in pharmacology · 2024Article
- A Potential Association between Ribonuclease 1 Dynamics in the Blood and the Outcome in COVID-19 Patients.International journal of molecular sciences · 2023Article
- Extracellular RNA Sensing Mediates Inflammation and Organ Injury in a Murine Model of Polytrauma.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Targeting neuro-immune systems to achieve cardiac tissue repair following myocardial infarction: A review of therapeutic approaches from in-vivo preclinical to clinical studies.Pharmacology & therapeutics · 2023Review
- Review
- Potential therapeutic strategies for myocardial infarction: the role of Toll-like receptors.Immunologic research · 2022Review
- TLR7 Mediates Acute Respiratory Distress Syndrome in Sepsis by Sensing Extracellular miR-146a.American journal of respiratory cell and molecular biology · 2022Article
- Brain innate immune response via miRNA-TLR7 sensing in polymicrobial sepsis.Brain, behavior, and immunity · 2022Article
- Article
- Targeting Toll-Like Receptors in Sepsis: From Bench to Clinical Trials.Antioxidants & redox signaling · 2021Review
- Secret messengers: Extracellular RNA communication in the immune system.Immunological reviews · 2021Review
- Chemokines in Myocardial Infarction.Journal of cardiovascular translational research · 2021Review
- Chemokines in cardiac fibrosis.Current opinion in physiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We have recently reported that extracellular RNA (exRNA) released from necrotic cells induces cytokine production in cardiomyocytes and immune cells and contributes to myocardial ischemia/reperfusion injury. However, the signaling mechanism by which exRNA exhibits its pro-inflammatory effect is unknown. Here we hypothesize that exRNA directly induces inflammation through specific Toll-like receptors (TLRs). To test the hypothesis, we treated rat neonatal cardiomyocytes, mouse bone marrow-derived macrophages (BMDM), or mouse neutrophils with RNA (2.5-10 μg/ml) isolated from rat cardiomyocytes or the hearts from mouse, rat, and human. We found that cellular RNA induced production of several cytokines such as macrophage inflammatory protein-2 (MIP-2), ILs, TNFα, and the effect was completely diminished by RNase, but not DNase. The RNA-induced cytokine production was partially inhibited in cells treated with TLR7 antagonist or genetically deficient in TLR7. Deletion of myeloid differentiation primary response protein 88 (MyD88), a downstream adapter of TLRs including TLR7, abolished the RNA-induced MIP-2 production. Surprisingly, genetic deletion of TLR3 had no impact on the RNA-induced MIP-2 response. Importantly, extracellular RNA released from damaged cardiomyocytes also induced cytokine production. Finally, mice treated with 50 μg of RNA intraperitoneal injection exhibited acute peritonitis as evidenced by marked neutrophil and monocyte migration into the peritoneal space. Together, these data demonstrate that exRNA of cardiac origin exhibits a potent pro-inflammatory property in vitro and in vivo and that exRNA induces cytokine production through TLR7-MyD88 signaling.
Indexed as
Identifiers
What OpenQuestion holds
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.