ArticleArteriosclerosis, thrombosis, and vascular biology2012
Endogenous IRAK-M attenuates postinfarction remodeling through effects on macrophages and fibroblasts.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Pooled it
- Meteorin-like regulates cardiac repair via macrophage modulation following myocardial infarction.Basic research in cardiology · 2026Article
- Plasma proteins and mechanisms involved in the evolvement of cardiac function after myocardial infarction.Scientific reports · 2026Article
- Single-Cell Insights Into Macrophage Subtypes in Pulmonary Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Post-myocardial Infarction Cardiac Remodeling: Multidimensional Mechanisms and Clinical Prospects of Stem Cell Therapy.Stem cell reviews and reports · 2025Review
- Macrophage Membrane-Coated Nanocarriers in Myocardial Infarction: A Paradigm Shift in Targeted Cardiac Therapy.International journal of nanomedicine · 2025Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Protective effects of macrophage-specific integrin α5 in myocardial infarction are associated with accentuated angiogenesis.Nature communications · 2023Article
- IRAK-M Regulates Proliferative and Invasive Phenotypes of Lung Fibroblasts.Inflammation · 2023Article
- IRAK-M suppresses the activation of microglial NLRP3 inflammasome and GSDMD-mediated pyroptosis through inhibiting IRAK1 phosphorylation during experimental autoimmune encephalomyelitis.Cell death & disease · 2023Article
- Myocardial injury: where inflammation and autophagy meet.Burns & trauma · 2023Review
- Macrophages in myocardial infarction.American journal of physiology. Cell physiology · 2022Review
- Prototype device for endoventricular beta-emitting radiotracer detection and molecularly-guided intervention.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2022Article
- Review
- Machine learning-based integration develops biomarkers initial the crosstalk between inflammation and immune in acute myocardial infarction patients.Frontiers in cardiovascular medicine · 2022Article
- Rapid Inflammasome Activation Is Attenuated in Post-Myocardial Infarction Monocytes.Frontiers in immunology · 2022Article
- [Platelet-rich plasma alleviates myocardial ischemia-reperfusion injury in rats].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- IRAK-M knockout promotes allergic airway inflammation, but not airway hyperresponsiveness, in house dust mite-induced experimental asthma model.Journal of thoracic disease · 2021Article
- Macrophage HIF-1α mediates obesity-related adipose tissue dysfunction via interleukin-1 receptor-associated kinase M.American journal of physiology. Endocrinology and metabolism · 2020Article
- Corosolic acid attenuates cardiac fibrosis following myocardial infarction in mice.International journal of molecular medicine · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveEffective postinfarction repair requires timely suppression of innate immune signals to prevent the catastrophic consequences of uncontrolled inflammation on cardiac geometry and function. In macrophages, interleukin-1 receptor-associated kinase (IRAK)-M acts as a functional decoy preventing uncontrolled toll-like receptor /interleukin-1-mediated responses. Our study investigates the role of IRAK-M as a negative regulator of the postinfarction inflammatory response and as a modulator of cardiac remodeling. METHODS AND
resultsIn wild-type mouse infarcts IRAK-M was upregulated in infiltrating macrophages and fibroblasts exhibiting a biphasic response. When compared with wild-type animals, infarcted IRAK-M(-/-) mice had enhanced adverse remodeling and worse systolic dysfunction; however, acute infarct size was comparable between groups. Adverse remodeling in IRAK-M(-/-) animals was associated with enhanced myocardial inflammation and protease activation. The protective actions of IRAK-M involved phenotypic modulation of macrophages and fibroblasts. IRAK-M(-/-) infarcts showed increased infiltration with proinflammatory CD11b+/Ly6C(hi) monocytes; leukocytes harvested from IRAK-M-null infarcts exhibited accentuated cytokine expression. In vitro, IRAK-M expression was upregulated in cytokine-stimulated murine cardiac fibroblasts and suppressed their matrix-degrading properties without affecting their inflammatory activity.
conclusionsEndogenous IRAK-M attenuates adverse postinfarction remodeling suppressing leukocyte inflammatory activity, while inhibiting fibroblast-mediated matrix degradation.
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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.