ArticleCirculation research2023
T-Cell MyD88 Is a Novel Regulator of Cardiac Fibrosis Through Modulation of T-Cell Activation.
Article in Circulation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Novel Quality Metrics for Assessing the Reproducibility and Translational Relevance of Mouse Transverse Aortic Constriction Experiments: A Systematic Review.Journal of the American Heart Association · 2026Pooled it
- Interleukin-18 armours antitumour immune effectors.Nature reviews. Immunology · 2026Review
- Microvascular endothelial scavenger receptor class B type I protects against heart failure with preserved ejection fraction by inhibiting T-cell cardiotropism.EMBO molecular medicine · 2026Article
- MyD88 Deficiency Protects Mice From Experimental Autoimmune Encephalomyelitis by Influencing Both Dendritic Cells and T Cells.Immunology · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Targeting of Cdc42-Interacting Protein 4-Calcineurin Signalosomes Improves Cardiac Structure and Function After Myocardial Infarction.Journal of the American Heart Association · 2026Article
- Migration of Cardiac Cells: Hot Topics that have not Attracted Clinical Attention.International journal of medical sciences · 2026Review
- When Resident Macrophages Call, Fibroblasts Answer: CCL24-CCR3 in Fibrosis.Circulation research · 2025Article
- Endothelial Cell Stimulator of Interferon Genes Regulates IL-6 Production and Is Required for Pathologic Cardiac Hypertrophy and Contractile Dysfunction in Experimental Heart Failure.The American journal of pathology · 2025Article
- PCSK9 Inhibitor Inclisiran Attenuates Cardiotoxicity Induced by Sequential Anthracycline and Trastuzumab Exposure via NLRP3 and MyD88 Pathway Inhibition.International journal of molecular sciences · 2025Article
- Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II-Induced Cardiac Hypertrophy.Journal of cellular and molecular medicine · 2025Article
- Experimental pressure overload induces a cardiac neoantigen specific humoral immune response.Journal of molecular and cellular cardiology · 2025Article
- Dynamic molecular atlas of cardiac fibrosis at single-cell resolution shows CD248 in cardiac fibroblasts orchestrates interactions with immune cells.Nature cardiovascular research · 2025Article
- Scaffold Proteins in Fibrotic Diseases of Visceral Organs.Biomolecules · 2025Review
- MyD88 determines T cell fate through BCAP-PI3K signaling.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Fibroblast-specific MyD88-dependent signaling aggravates inflammation and cardiac dysfunction in the MI heart.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration.Nature cardiovascular research · 2024Article
- Cytotoxic T cells drive doxorubicin-induced cardiac fibrosis and systolic dysfunction.Nature cardiovascular research · 2024Article
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Intersection of Immunology and Metabolism in Myocardial Disease.Circulation research · 2024Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundCardiac inflammation in heart failure is characterized by the presence of damage-associated molecular patterns, myeloid cells, and T cells. Cardiac damage-associated molecular patterns provide continuous proinflammatory signals to myeloid cells through TLRs (toll-like receptors) that converge onto the adaptor protein MyD88 (myeloid differentiation response 88). These induce activation into efficient antigen-presenting cells that activate T cells through their TCR (T-cell receptor). T-cell activation results in cardiotropism, cardiac fibroblast transformation, and maladaptive cardiac remodeling. T cells rely on TCR signaling for effector function and survival, and while they express MyD88 and damage-associated molecular pattern receptors, their role in T-cell activation and cardiac inflammation is unknown.
methodsWe performed transverse aortic constriction in mice lacking MyD88 in T cells and analyzed remodeling, systolic function, survival, and T-cell activation. We profiled wild type versus
resultsAnalysis of single-cell RNA-sequencing data sets revealed that MyD88 is expressed in mouse and human cardiac T cells. MyD88 deletion in T cells resulted in increased levels of cardiac T-cell infiltration and fibrosis in response to transverse aortic constriction. We discovered that TCR-activated
conclusionsOur results outline a novel intrinsic role for MyD88 in limiting T-cell activation that is central to tune down cardiac inflammation during cardiac adaptation to stress.
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Registered trials
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