ArticleCardiovascular research2014
CXCR3-independent actions of the CXC chemokine CXCL10 in the infarcted myocardium and in isolated cardiac fibroblasts are mediated through proteoglycans.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 71 citations in OpenAlex.
- 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
- Lung-Derived Small Extracellular Vesicles Containing miR-15a-5p/miR-96-5p Promote Myocardial Fibrosis in Hypertrophic Cardiomyopathy via Targeting SMAD7.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Intersection of Cardio-Oncology: An Overview of Radiation-Induced Heart Disease in the Context of Tumors.Journal of the American Heart Association · 2025Review
- CXCR3-independent role of CXCL10 in alveolar epithelial repair.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- The roles of Th cells in myocardial infarction.Cell death discovery · 2024Review
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Esaxerenone Protects against Diabetic Cardiomyopathy via Inhibition of the Chemokine and PI3K-Akt Signaling Pathway.Biomedicines · 2023Article
- A review of the pleiotropic actions of the IFN-inducible CXC chemokine receptor 3 ligands in the synovial microenvironment.Cellular and molecular life sciences : CMLS · 2023Review
- Pathophysiological impact of CXC and CX3CL1 chemokines in preeclampsia and gestational diabetes mellitus.Frontiers in cell and developmental biology · 2023Review
- Review
- CXCL10 is a novel anti-angiogenic factor downstream of p53 in cardiomyocytes.Physiological reports · 2022Article
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Chemokines in cardiac fibrosis.Current opinion in physiology · 2021Article
- Chemokines in Myocardial Infarction.Journal of cardiovascular translational research · 2021Review
- Cardiac Immunology: A New Era for Immune Cells in the Heart.Advances in experimental medicine and biology · 2021Review
- Dephosphorylation of Caveolin-1 Controls C-X-C Motif Chemokine Ligand 10 Secretion in Mesenchymal Stem Cells to Regulate the Process of Wound Healing.Frontiers in cell and developmental biology · 2021Article
- Immune regulation of cardiac fibrosis post myocardial infarction.Cellular signalling · 2021Review
- Adding insult to injury - Inflammation at the heart of cardiac fibrosis.Cellular signalling · 2021Review
- T-cell regulation of fibroblasts and cardiac fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- Potential therapeutic manipulations of the CXCR3 chemokine axis for the treatment of inflammatory fibrosing diseases.F1000Research · 2020Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
aimsThe CXC chemokine CXCL10 is up-regulated in the infarcted myocardium and limits cardiac fibrosis by inhibiting growth factor-mediated fibroblast migration. CXCL10 signals by binding to its receptor CXCR3; however, recently CXCR3-independent CXCL10 actions have been suggested. Our study explores the role of CXCR3 signalling in myocardial infarction and investigates its involvement in mediating the anti-fibrotic effects of CXCL10. METHODS AND
resultsWild-type and CXCR3 null mice underwent reperfused infarction protocols. CXCL10 was markedly induced in the infarct; in contrast, expression of the other two CXCR3 ligands, CXCL9 and CXCL11 was extremely low. CXCR3 loss did not affect scar size, geometric ventricular remodelling, collagen deposition, and systolic dysfunction of the infarcted heart. CXCR3 null mice had increased peak neutrophil recruitment and delayed myofibroblast infiltration in the infarcted heart, but exhibited comparable myocardial expression of pro-inflammatory cytokines and chemokines. In vitro, CXCL10 did not modulate Transforming Growth Factor (TGF)-β signalling, but inhibited basic fibroblast growth factor (bFGF)-induced cardiac fibroblast migration in both wild-type and CXCR3 null cells. Treatment of fibroblasts with heparinase and chondroitinase to cleave glycosaminoglycan chains abrogated the inhibitory effects of CXCL10 on cell migration.
conclusionCXCR3 signalling does not critically regulate cardiac remodelling and dysfunction following myocardial infarction. The anti-fibrotic effects of CXCL10 in the healing infarct and in isolated cardiac fibroblasts are CXCR3-independent and may be mediated through proteoglycan signalling. Thus, administration of CXCR3-defective forms of CXCL10 may be an effective anti-fibrotic strategy in the remodelling myocardium without activating a potentially injurious, CXCR3-driven T cell response.
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