ArticleThe American journal of pathology2010
CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory T cells.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers.
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Who cites it
171 citing papers in PubMed, 290 citations in OpenAlex.
- Effect of ciclosporin on safety, lymphocyte kinetics and left ventricular remodelling in acute myocardial infarction.British journal of clinical pharmacology · 2020Trial
- Meteorin-like regulates cardiac repair via macrophage modulation following myocardial infarction.Basic research in cardiology · 2026Article
- Role of Inflammation in the Development of Heart Failure After Myocardial Infarction.Reviews in cardiovascular medicine · 2026Review
- Macrophage-Dependent Intercellular Crosstalk in Multiphenotypic Heart Failure With Preserved Ejection Fraction.Journal of the American Heart Association · 2026Review
- Article
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Immune Mechanisms in Myocardial Remodeling Following Myocardial Infarction: Focusing on Regulatory Networks of T Cell Responses.Journal of inflammation research · 2026Review
- Molecular Crosstalk Between Intrauterine hCG and Endometrial Receptivity: Signalling Pathways, Immune Modulation, and Translational Perspectives in IVF.International journal of molecular sciences · 2025Review
- The spatial and temporal activation of macrophages during fibrosis.Nature reviews. Immunology · 2025Review
- Beyond CYP2C19: inflammation and angiogenesis gene variants drive clopidogrel resistance in CAD patients.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Pattern of Regulatory T Cells, Resident Memory T Cells, and Exhausted T Cells in Human Pericardial Fluid Samples of Cardiovascular Patients.International journal of molecular sciences · 2025Article
- Advances in fibroblast-based cardiac reprogramming in the treatment of heart disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Metabolic and transcriptomic insights into temperature controlled hypothermic preservation of human donor hearts.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2025Article
- Post-myocardial Infarction Cardiac Remodeling: Multidimensional Mechanisms and Clinical Prospects of Stem Cell Therapy.Stem cell reviews and reports · 2025Review
- Use of regulatory cells for achieving functional tolerance of pig heart xenotransplants in humans: a literature review.Frontiers in immunology · 2025Review
- The dual role of tissue regulatory T cells in tissue repair: return to homeostasis or fibrosis.Frontiers in immunology · 2025Review
- Article
- Exploring CCR5 + T regulatory cell subset dysfunction in type 1 diabetes patients: implications for immune regulation.Immunologic research · 2024Article
- Regulatory T Cells in Pathological Cardiac Hypertrophy: Mechanisms and Therapeutic Potential.Cardiovascular drugs and therapy · 2024Review
- The role of regulatory T cells in vitiligo and therapeutic advances: a mini-review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
111 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Myocardial infarction triggers an inflammatory reaction that is involved in cardiac remodeling. Cardiac repair is dependent on regulatory mechanisms that suppress inflammation and prevent excessive matrix degradation. Chemokine induction in the infarcted heart mediates recruitment of leukocyte subsets with distinct properties. We demonstrate that signaling through the CC chemokine receptor 5 (CCR5) prevents uncontrolled postinfarction inflammation and protects from adverse remodeling by recruiting suppressive mononuclear cells. CCR5 and its ligands macrophage inflammatory protein (MIP)-1alpha and MIP-1beta were markedly induced in the infarcted mouse myocardium. In addition, almost 40% of the mononuclear cells infiltrating the infarct expressed CCR5. CCR5(-/-) mice exhibited marked upregulation of proinflammatory cytokine and chemokine expression in the infarct. In wild-type infarcts CCR5+ mononuclear cells had anti-inflammatory properties, expressing higher levels of IL-10 than CCR5- cells. In contrast, mononuclear cells isolated from CCR5(-/-) infarcts had reduced IL-10 expression. Moreover, enhanced inflammation in the absence of CCR5 was associated with impaired recruitment of CD4+/foxp3+ regulatory T cells (Tregs). The CCR5+ Treg subset exhibited increased IL-10 expression, reflecting potent anti-inflammatory activity. Accentuated inflammation in CCR5(-/-) infarcts was associated with increased matrix metalloproteinase (MMP) expression, reduced TIMP levels, and enhanced MMP-2 and MMP-9 activity, resulting in worse cardiac dilation. These results suggest that CCR5-mediated Treg recruitment may restrain postinfarction inflammation, preventing excessive matrix degradation and attenuating adverse remodeling.
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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.