ArticleNature communications2021
Cardiac macrophages prevent sudden death during heart stress.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 98 citations in OpenAlex.
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Altered bone marrow niche forms central innate immune memory driving cardiac dysfunction.Nature communications · 2026Article
- The Immune System as a Proarrhythmic Mediator: A Novel Paradigm for the Development of New Antiarrhythmic Therapy.The Canadian journal of cardiology · 2026Review
- Review
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- Mapping the miRNA landscape of primitive macrophage extracellular vesicles highlights their pro-vasculogenic effects in engineered human cardiac tissue.APL bioengineering · 2026Article
- Review
- Low-Dose Cardiac Radiation Improves Electrical Function and Reduces Ventricular Arrhythmogenesis in Mice With Nonischemic Cardiomyopathy.JACC. Clinical electrophysiology · 2026Article
- Amphiregulin attenuates sepsis-induced myocardial dysfunction by maintaining the localization of connexin43.Inflammation and regeneration · 2026Article
- Gap junctional and ephaptic coupling in cardiac electrical propagation: homocellular and heterocellular perspectives.The Journal of physiology · 2026Review
- Cardiac resident macrophages: the emerging role in arrhythmogenesis.Frontiers in immunology · 2026Review
- The role of macrophages in cardiac diseases: a review of the origins, functional diversity, and therapeutic potential.Frontiers in immunology · 2026Review
- A Macrophage-Derived Factor on Human iPSC-Derived Cardiomyocyte Function: The Role of Osteopontin.Cells · 2025Article
- Advancements in nanomedicine for modulating ischemic cardiomyopathy therapy.Materials today. Bio · 2025Review
- Immune Cell Dynamics in Cardiac Diseases: Insights From Single-Cell Sequencing.Journal of cellular and molecular medicine · 2025Review
- Modulation of Macrophage Polarization by Traditional Chinese Medicine in HFpEF: A Review of Mechanisms and Therapeutic Potentials.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025Review
- Cardiac macrophage: Insights from murine models to translational potential for human studies.Journal of molecular and cellular cardiology · 2025Review
- AREGMolecular medicine (Cambridge, Mass.) · 2025Article
- Article
6 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
20 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac arrhythmias are a primary contributor to sudden cardiac death, a major unmet medical need. Because right ventricular (RV) dysfunction increases the risk for sudden cardiac death, we examined responses to RV stress in mice. Among immune cells accumulated in the RV after pressure overload-induced by pulmonary artery banding, interfering with macrophages caused sudden death from severe arrhythmias. We show that cardiac macrophages crucially maintain cardiac impulse conduction by facilitating myocardial intercellular communication through gap junctions. Amphiregulin (AREG) produced by cardiac macrophages is a key mediator that controls connexin 43 phosphorylation and translocation in cardiomyocytes. Deletion of Areg from macrophages led to disorganization of gap junctions and, in turn, lethal arrhythmias during acute stresses, including RV pressure overload and β-adrenergic receptor stimulation. These results suggest that AREG from cardiac resident macrophages is a critical regulator of cardiac impulse conduction and may be a useful therapeutic target for the prevention of sudden death.
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.