Hypoxia Induces M2 Macrophages to Express VSIG4 and Mediate Cardiac Fibrosis After Myocardial Infarction

Wang, Yan; Zhang, Yu; Li, Jiao; Li, Chaofu; Zhao, Ranzun; Shen, Changyin; Liu, Weiwei; Rong, Jidong; Wang, Zhenglong; Ge, Junbo; Shi, Bei

doi:10.7150/thno.78736

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Theranostics 2023; 13(7):2192-2209. doi:10.7150/thno.78736 This issue Cite

Research Paper

Hypoxia Induces M2 Macrophages to Express VSIG4 and Mediate Cardiac Fibrosis After Myocardial Infarction

Yan Wang^1,2#, Yu Zhang^1#, Jiao Li^1#, Chaofu Li¹, Ranzun Zhao¹, Changyin Shen¹, Weiwei Liu¹, Jidong Rong¹, Zhenglong Wang^1✉, Junbo Ge^3✉, Bei Shi^1,2✉

1. Department of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China
2. Soochow University, Suzhou, China
3. Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China
^#These authors contributed to this work equally

Citation:

Wang Y, Zhang Y, Li J, Li C, Zhao R, Shen C, Liu W, Rong J, Wang Z, Ge J, Shi B. Hypoxia Induces M2 Macrophages to Express VSIG4 and Mediate Cardiac Fibrosis After Myocardial Infarction. Theranostics 2023; 13(7):2192-2209. doi:10.7150/thno.78736. https://www.thno.org/v13p2192.htm

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Abstract

M2 macrophage-mediated tissue repair plays an important role in acute myocardial infarction (AMI). Additionally, VSIG4, which is mainly expressed on tissue-resident and M2 macrophages, is crucial for the regulation of immune homeostasis; however, its effects on AMI remain unknown. In this study, we aimed to investigate the functional significance of VSIG4 in AMI using VSIG4 knockout and adoptive bone marrow transfer chimeric models. We also determined the function of cardiac fibroblasts (CFs) through gain- or loss-of-function experiments. We showed that VSIG4 promotes scar formation and orchestrates the myocardial inflammatory response after AMI, while also promoting TGF-β1 and IL-10. Moreover, we revealed that hypoxia promotes VSIG4 expression in cultured bone marrow M2 macrophages, ultimately leading to the conversion of CFs to myofibroblasts. Our results reveal a crucial role for VSIG4 in the process of AMI in mice and provide a potential immunomodulatory therapeutic avenue for fibrosis repair after AMI.

Keywords: Myocardial infarction, Hypoxia, Macrophages, VSIG4, Cardiac fibrosis

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APA

Wang, Y., Zhang, Y., Li, J., Li, C., Zhao, R., Shen, C., Liu, W., Rong, J., Wang, Z., Ge, J., Shi, B. (2023). Hypoxia Induces M2 Macrophages to Express VSIG4 and Mediate Cardiac Fibrosis After Myocardial Infarction. Theranostics, 13(7), 2192-2209. https://doi.org/10.7150/thno.78736.

ACS

Wang, Y.; Zhang, Y.; Li, J.; Li, C.; Zhao, R.; Shen, C.; Liu, W.; Rong, J.; Wang, Z.; Ge, J.; Shi, B. Hypoxia Induces M2 Macrophages to Express VSIG4 and Mediate Cardiac Fibrosis After Myocardial Infarction. Theranostics 2023, 13 (7), 2192-2209. DOI: 10.7150/thno.78736.

NLM

CSE

Wang Y, Zhang Y, Li J, Li C, Zhao R, Shen C, Liu W, Rong J, Wang Z, Ge J, Shi B. 2023. Hypoxia Induces M2 Macrophages to Express VSIG4 and Mediate Cardiac Fibrosis After Myocardial Infarction. Theranostics. 13(7):2192-2209.

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