ArticleCell biology and toxicology2023
CCL24/CCR3 axis plays a central role in angiotensin II-induced heart failure by stimulating M2 macrophage polarization and fibroblast activation.
Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 34 citations in OpenAlex.
- Heart Failure with Reduced versus Preserved Ejection Fraction: Molecular Mechanisms, Immunologic Pathways, Current Therapies, and Future Directions.Archives of internal medicine research · 2026Article
- Dose-Dependent Alterations in Lung Immune Subpopulations in Influenza a Virus Infection.International journal of molecular sciences · 2026Article
- Spironolactone and Fibrosis in Heart Failure Risk: Machine Learning Analysis of HOMAGE Trial Plasma Proteomics.MedComm · 2026Article
- Integrated analysis of cell-in-cell related genes and immune microenvironment in heart failure.Frontiers in cell and developmental biology · 2026Article
- A Macrophage/Monocyte-Related Four-Gene Signature for Prognostic Assessment of Uveal Melanoma:Human mutation · 2026Article
- Quorum sensing geneFrontiers in microbiology · 2026Article
- CCL24 recruits CCR3International journal of biological sciences · 2026Article
- PPARα-Mediated Fatty Acid Catabolism in Astrocytes Was Involved in Improvement of Cognitive Dysfunction by Phlorizin in APP/PS1 Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Macrophage-Derived CCL24 Promotes Cardiac Fibrosis Via Fibroblast CCR3.Circulation research · 2025Article
- When Resident Macrophages Call, Fibroblasts Answer: CCL24-CCR3 in Fibrosis.Circulation research · 2025Article
- Silencing of lncRNA Gm26917 Attenuates Alveolar Macrophage-mediated Inflammatory Response in LPS-induced Acute Lung Injury Via Inhibiting NKRF Ubiquitination.Inflammation · 2025Article
- Macrophage Containing Cardiac Organoids for Studying Inflammatory Programmes Driving Cardiovascular Disease.Current cardiology reports · 2025Review
- Review
- Reciprocal activation between M1 macrophages and trophoblasts through CXCL9/STAT1/ZEB1/CCL2 axis promotes recurrent spontaneous abortion.Frontiers in immunology · 2025Article
- Inflammatory and fibrotic signaling pathways mediated by cardiac macrophages in atrial fibrillation.Frontiers in cardiovascular medicine · 2025Review
- Influence of secretome from porcine cardiosphere-derived cells on porcine macrophage polarization and their possible implications for cardiac remodeling post-myocardial infarctionFrontiers in cell and developmental biology · 2025Article
- OGT-mediated O-GlcNAcylation regulates macrophage polarization in heart failure via targeting IRF1.BMC cardiovascular disorders · 2024Article
- MiR-21-3p inhibitor exerts myocardial protective effects by altering macrophage polarization state and reducing excessive mitophagy.Communications biology · 2024Article
- Sulfenylation of ERK1/2: A novel mechanism for SOHeliyon · 2024Article
- Osteoprotegerin Is Essential for the Development of Endothelial Dysfunction Induced by Angiotensin II in Mice.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsWe aimed to investigate the effect and mechanism of pleiotropic chemokine CCL24 in heart failure. METHODS AND
resultsCompared with normal donators, the expression of CCL24 and number of cardiac M2 macrophages in heart were higher in heart failure patients, the same as plasma CCL24. Treatment with CCL24 antibody hindered Ang II (1500 ng/kg/min)-induced cardiac adverse remodeling through preventing cardiac hypertrophy and fibrosis. RNA-seq showed that CCL24/CCR3 axis was involved in immune and inflammatory responses. Single-cell analysis of cytometry by time of flight (CyTOF) revealed that CCL24 antibody decreased the M2 macrophage and monocyte polarization during Ang II stimulation. Immunofluorescence co-localization analysis confirmed the expression of CCR3 in macrophage and fibroblasts. Then, in vitro experiments confirmed that CCL24/CCR3 axis was also involved in cardiac primary fibroblast activation through its G protein-coupled receptor function.
conclusionCCL24/CCR3 axis plays a crucial part in cardiac remodeling by stimulating M2 macrophage polarization and cardiac fibroblast activation. Cardiac M2 macrophages, CCL24 and circulation CCL24 increased in heart failure patients. Treatment with CCL24 Ab hindered Ang II induced cardiac structural dysfunction and electrical remodeling. In CCL24 Ab group RNA-seq found that it was related to immune responses and hypertrophic cardiomyopathy, CytoF revealed M2 macrophages and monocytes decreased obviously. In vitro,CCL24 promoted activation and migration of cardiac fibroblast.
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