ReviewJACC. Basic to translational science2020
Innate Immune Receptors, Key Actors in Cardiovascular Diseases.
Review in JACC. Basic to translational science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.
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
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.
- Efficacy and safety of empagliflozin for the acute myocardial infarction: a systematic review and meta-analysis of randomized controlled trials.Annals of medicine · 2025Pooled it
- Immune Tolerance vs. Immune Resistance: The Interaction Between Host and Pathogens in Infectious Diseases.Frontiers in veterinary science · 2022Pooled it
- Gut-derived bacterial extracellular vesicles: the microbial dark matter contributing to host inflammation and cardiometabolic disease.Gut microbes · 2026Review
- Toll-like receptor 7 constrains efferocytosis in myocardial injury.Basic research in cardiology · 2026Article
- Plasma proteomics stratification identifies phospholamban R14del carriers at risk for disease progression.Cardiovascular research · 2026Article
- Hematopoietic expression of cIAP2 drives inflammation and heart failure after myocardial infarction.Nature cardiovascular research · 2026Article
- TLR7 inhibition limits cardiac ischemic injury by disrupting ITGAM-dependent immune-endothelial interaction.bioRxiv : the preprint server for biology · 2026Article
- NOD1 is a key mediator of atrial myopathy in heart failure.Theranostics · 2026Article
- Protective role of the C-reactive protein-albumin-lymphocyte (CALLY) index for cardiovascular risk and mortality.Scientific reports · 2025Article
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- Atrial Myopathy and Heart Failure: Immunomolecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2025Review
- Prevalence and clinical risk factors of cardiovascular disease in patients with cancer: a cross-sectional study.BMC cardiovascular disorders · 2025Article
- ADAM8 deficiency in macrophages promotes cardiac repair after myocardial infarction via ANXA2-mTOR-autophagy pathway.Journal of advanced research · 2025Article
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- Stimuli-Responsive Nanomedicines for the Treatment of Non-cancer Related Inflammatory Diseases.ACS nano · 2025Review
- Review
- Computational analysis of antimicrobial peptides targeting key receptors in infection-related cardiovascular diseases: molecular docking and dynamics insights.Scientific reports · 2025Article
- Identification of regulator gene and pathway in myocardial ischemia-reperfusion injury: a bioinformatics and biological validation study.Hereditas · 2025Article
- Article
- Macrophage Membrane-Coated Nanocarriers in Myocardial Infarction: A Paradigm Shift in Targeted Cardiac Therapy.International journal of nanomedicine · 2025Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases (CVDs) are the leading cause of death in the industrialized world. Most CVDs are associated with increased inflammation that arises mainly from innate immune system activation related to cardiac damage. Sustained activation of the innate immune system frequently results in maladaptive inflammatory responses that promote cardiovascular dysfunction and remodeling. Much research has focused on determining whether some mediators of the innate immune system are potential targets for CVD therapy. The innate immune system has specific receptors-termed pattern recognition receptors (PRRs)-that not only recognize pathogen-associated molecular patterns, but also sense danger-associated molecular signals. Activation of PRRs triggers the inflammatory response in different physiological systems, including the cardiovascular system. The classic PRRs, toll-like receptors (TLRs), and the more recently discovered nucleotide-binding oligomerization domain-like receptors (NLRs), have been recently proposed as key partners in the progression of several CVDs (e.g., atherosclerosis and heart failure). The present review discusses the key findings related to the involvement of TLRs and NLRs in the progression of several vascular and cardiac diseases, with a focus on whether some NLR subtypes (nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain-containing receptor 3 and nucleotide-binding oligomerization domain-containing protein 1) can be candidates for the development of new therapeutic strategies for several CVDs.
Indexed as
Identifiers
What Socratic 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 Socratic graph.