ArticleImmunity, inflammation and disease2024
CXCL4/CXCR3 axis regulates cardiac fibrosis by activating TGF-β1/Smad2/3 signaling in mouse viral myocarditis.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 9 citations in OpenAlex.
- Effect of LY2109761 on TGF-β1/TGFβRI/Smad Pathway and Hepatic Fibrosis Cysts Formation in Rats Infected with Echinococcus granulosus: an In Vitro and In Vivo Study.Acta parasitologica · 2026Article
- [Research progress on the pathogenesis and clinical treatment of cirrhotic cardiomyopathy].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Mast Cell-Derived CXCL4: A Key Mediator of Ferroptosis and Cardiac Damage in Septic Cardiomyopathy.Immunity, inflammation and disease · 2026Article
- Therapeutic Targeting of Viral Myocarditis with Natural Products and Herbal Medicines: From Immune-Inflammatory Mechanisms to Clinical Translation.Journal of inflammation research · 2026Review
- Myocardial inflammation in myocarditis: mechanisms and therapeutic targets.Frontiers in cardiovascular medicine · 2026Review
- Review
- Thermal tolerance of turbot based on cardiac performance and analysis of molecular regulatory mechanisms.Fish physiology and biochemistry · 2025Article
- Muscone Attenuates Uveitis Through the PI3K/AKT Signaling Pathway.Investigative ophthalmology & visual science · 2025Article
- Comprehensive Analysis of Differences in N6-Methyladenosine RNA Methylation Groups in CVB3-Induced Viral Myocarditis and Identification of the Anti-Apoptotic Role of RBM15B.Journal of inflammation research · 2025Article
- Platelet Factor 4: A Mysterious Chemokine in Inflammatory Regulation Diseases.Journal of inflammation research · 2025Review
- The Cardiomyocyte in Cirrhosis: Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy.Reviews in cardiovascular medicine · 2024Review
- CXCL4/CXCR3 axis regulates cardiac fibrosis by activating TGF-β1/Smad2/3 signaling in mouse viral myocarditis.Immunity, inflammation and disease · 2024Article
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6 authors at 2 institutions in 1 country.
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Abstract
backgroundSevere myocarditis is often accompanied by cardiac fibrosis, but the underlying mechanism has not been fully elucidated. CXCL4 is a chemokine that has been reported to have pro-inflammatory and profibrotic functions. The exact role of CXCL4 in cardiac fibrosis remains unclear.
methodsViral myocarditis (VMC) models were induced by intraperitoneal injection of Coxsackie B Type 3 (CVB3). In vivo, CVB3 (100 TCID50) and CVB3-AMG487 (CVB3: 100 TCID50; AMG487: 5 mg/kg) combination were administered in the VMC and VMC+AMG487 groups, respectively. Hematoxylin and eosin staining, severity score, Masson staining, and immunofluorescence staining were performed to measure myocardial morphology in VMC. Enzyme-linked immunosorbent assay (ELISA) and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were performed to quantify inflammatory factors (IL-1β, IL-6, TNF-α, and CXCL4). Aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine kinase-myocardial band (CK-MB) levels were analyzed by commercial kits. CXCL4, CXCR3B, α-SMA, TGF-β1, Collagen I, and Collagen III were determined by Western blot and immunofluorescence staining.
resultsIn vivo, CVB3-AMG487 reduced cardiac injury, α-SMA, Collagen I and Collagen III levels, and collagen deposition in VMC+AMG487 group. Additionally, compared with VMC group, VMC+AMG group decreased the levels of inflammatory factors (IL-1β, IL-6, and TNF-α). In vitro, CXCL4/CXCR3B axis activation TGF-β1/Smad2/3 pathway promote mice cardiac fibroblasts differentiation.
conclusionCXCL4 acts as a profibrotic factor in TGF-β1/Smad2/3 pathway-induced cardiac fibroblast activation and ECM synthesis, and eventually progresses to cardiac fibrosis. Therefore, our findings revealed the role of CXCL4 in VMC and unveiled its underlying mechanism. CXCL4 appears to be a potential target for the treatment of VMC.
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