Viral myocarditis (VMC) is characterized by cardiac inflammation and excessive inflammatory responses after viral infection. SENP2, a deSUMO-specific protease, has been reported to regulate antiviral innate immunity. This study aimed to investigate whether SENP2 affects CVB3-induced VMC. We generated a CVB3-induced VMC mouse model in 6-week-old cardiomyocyte-specific Senp2 knockout mice. The mice were sacrificed at days 0, 2, 4 and 6 after CVB3 infection. The survival rate, body weight, myocardial histopathological changes, viral load, cytokine levels and antiviral gene expression in cardiac tissues of both groups were investigated. Our study indicated that the expression of Senp2 in primary cardiomyocytes was upregulated by CVB3 infection. Moreover, deletion of Senp2 in the heart exacerbated CVB3 infection-induced myocarditis, facilitated CVB3 viral replication and downregulated the expression of antiviral proteins. In conclusion, our findings suggest a protective role for SENP2 in CVB3-induced VMC.
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http://dx.doi.org/10.1016/j.intimp.2020.106941 | DOI Listing |
Immun Inflamm Dis
November 2024
Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Background: Viral myocarditis (VMC) plays a significant role in heart failure, and there is currently a shortage of available targeted treatments. Macrophage phenotype and function are closely associated with the beta-2 adrenergic receptor (β2-AR).
Method: This research employed a BALB/c mouse model of VMC generated using Coxsackievirus B3 (CVB3), and the β2-AR agonist formoterol was administered as treatment.
Int Immunopharmacol
December 2024
Department of Cardiology, Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China. Electronic address:
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.
View Article and Find Full Text PDFCardiovasc Toxicol
December 2024
Department of Cardiology, The Affiliated Children's Hospital of Xiangya School of Medicine, Central South University (Hunan Children's Hospital), No. 86 Ziyuan Road, Yuhua District, Changsha, Hunan, 410007, People's Republic of China.
Viral myocarditis (VMC) is an inflammatory disease of the myocardium caused by cardioviral infection, especially coxsackievirus B3 (CVB3), and is a major contributor to acute heart failure and sudden cardiac death in children and adolescents. LncRNA MALAT1 knockdown reportedly inhibits the differentiation of Th17 cells to attenuate CVB3-induced VMC in mice. Moreover, long non-coding RNAs (lncRNAs) interact with RNA-binding proteins (RBPs) to regulate UPF1-mediated mRNA decay.
View Article and Find Full Text PDFJ Zhejiang Univ Sci B
May 2024
Department of Pediatric Pulmonology and Immunology, West China Second University Hospital, Sichuan University, Chengdu 610041, China.
Viral myocarditis (VMC) is one of the most common acquired heart diseases in children and teenagers. However, its pathogenesis is still unclear, and effective treatments are lacking. This study aimed to investigate the regulatory pathway by which exosomes alleviate ferroptosis in cardiomyocytes (CMCs) induced by coxsackievirus B3 (CVB3).
View Article and Find Full Text PDFInt Immunopharmacol
May 2024
Department of Laboratory Medicine, Jiangning Hospital Affiliated to Nanjng Medical University, Nanjing 211100, China; Department of Laboratory Medicine, Nanjing First Hospital, Nanjng Medical University, Nanjing 210006, China. Electronic address:
Severe myocarditis is often accompanied by cardiac fibrosis, but the underlying mechanism has not been fully elucidated. NOD-like receptor protein 3 (NLRP3) inflammation is involved in the development of myocarditis and is closely related to the form of cell death. Inhibiting pyroptosis mediated by NLRP3 inflammasome can reduce cardiac fibrosis, although its exact mechanism remains unknown.
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