科研成果详情

题名Macrophage-derived VEGF-C reduces cardiac inflammation and prevents heart dysfunction in CVB3-induced viral myocarditis via remodeling cardiac lymphatic vessels
作者
发表日期2024-12-25
发表期刊International Immunopharmacology   影响因子和分区
语种英语
原始文献类型Article
关键词Cardiac lymphangiogenesis Viral mycarditis Inflammation Macrophage VEGF-C
其他关键词GROWTH-FACTOR ; LYMPHANGIOGENESIS
摘要Background: Cardiac lymphatic vessels are important channels for cardiac fluid circulation and immune regulation. In myocardial infarction and chronic heart failure, promoting cardiac lymphangiogenesis is beneficial in reducing cardiac edema and inflammation. However, the specific involvement of cardiac lymphangiogenesis in viral myocarditis (VMC) has not been studied. Despite the recognized participation of macrophages in lymphangiogenesis, the contribution of macrophages to cardiac lymphangiogenesis in VMC is still unclear. Methods: The male Balb/c mice with VMC were grouped according to the time to explore changes in inflammation, cardiac function and lymphangiogenesis. Adeno-associated virus (AAV) was used to determine the effect of cardiac lymphangiogenesis in VMC. Macrophage depletion and VEGF-CC156S treatment were used to investigate the connection between macrophages and cardiac lymphangiogenesis. Results: Cardiac inflammation and lymphatic vessel density were both upregulated, peaking on day 7 following CVB3 infection. After treatment with AAV-sVEGFR3, lymphangiogenesis was inhibited, leading to worsened cardiac dysfunction and aggravated inflammation. However, these effects were reversed by AAV-VEGF-C treatment. Furthermore, macrophages infiltrated the inflamed myocardium and secreted VEGF-C. In vitro, VEGF-C was upregulated when RAW264.7 cells were co-cultured with CVB3. Macrophage depletion in mice with VMC inhibited lymphangiogenesis, while supplementation with VEGF-CC156S depressed it. Conclusion: Collectively, these results indicate that activation of the VEGF-C/VEGFR3 axis exerts a protective effect in CVB3-induced VMC by resolving inflammation and alleviating cardiac dysfunction through increased lymphatic vasculature density, with macrophage-derived VEGF-C partially contributing to this effect.
资助项目Key Program of Natural Science Foundation of Zhejiang Province [LY22H020009]
出版者ELSEVIER
ISSN1567-5769
EISSN1878-1705
卷号143期号:Pt 1
DOI10.1016/j.intimp.2024.113377
页数13
WOS类目Immunology ; Pharmacology & Pharmacy
WOS研究方向Immunology ; Pharmacology & Pharmacy
WOS记录号WOS:001336150300001
收录类别SCIE ; SCOPUS ; PUBMED
URL查看原文
PubMed ID39405931
SCOPUSEID2-s2.0-85206260738
通讯作者地址[Li, Yue-Chun]Wenzhou Med Univ, Affiliated Hosp 2, Dept Cardiol, Wenzhou, Peoples R China. ; [Zhang, Wen-Wu;Li, Yue-Chun]Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou, Peoples R China. ; [Zhang, Wen-Wu]Wenzhou Med Univ, Affiliated Hosp 2, Dept Intens Care Unit, Wenzhou, Peoples R China.
Scopus学科分类Immunology and Allergy;Immunology;Pharmacology
SCOPUS_IDSCOPUS_ID:85206260738
引用统计
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/220818
专题附属第二医院
附属第二医院_耳鼻咽喉科
第二临床医学院、附属第二医院、育英儿童医院
附属第二医院_重症医学科
通讯作者Zhang, Wen-Wu; Li, Yue-Chun
作者单位
1.Wenzhou Med Univ, Affiliated Hosp 2, Dept Cardiol, Wenzhou, Peoples R China;
2.Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou, Peoples R China;
3.Wenzhou Med Univ, Affiliated Hosp 2, Dept Intens Care Unit, Wenzhou, Peoples R China
第一作者单位附属第二医院;  第二临床医学院,附属第二医院、育英儿童医院;  耳鼻咽喉科
通讯作者单位附属第二医院;  第二临床医学院,附属第二医院、育英儿童医院;  耳鼻咽喉科;  重症医学科
第一作者的第一单位附属第二医院
推荐引用方式
GB/T 7714
Chen, Yi-Lian,Lin, Yuan-Nan,Xu, Jing,et al. Macrophage-derived VEGF-C reduces cardiac inflammation and prevents heart dysfunction in CVB3-induced viral myocarditis via remodeling cardiac lymphatic vessels[J]. International Immunopharmacology,2024,143(Pt 1).
APA Chen, Yi-Lian., Lin, Yuan-Nan., Xu, Jing., Qiu, Yi-Xuan., Wu, Yi-Hao., ... & Li, Yue-Chun. (2024). Macrophage-derived VEGF-C reduces cardiac inflammation and prevents heart dysfunction in CVB3-induced viral myocarditis via remodeling cardiac lymphatic vessels. International Immunopharmacology, 143(Pt 1).
MLA Chen, Yi-Lian,et al."Macrophage-derived VEGF-C reduces cardiac inflammation and prevents heart dysfunction in CVB3-induced viral myocarditis via remodeling cardiac lymphatic vessels".International Immunopharmacology 143.Pt 1(2024).

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