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Coxsackievirus B3 regulates macrophage polarization through ANXA3 to promote the development of myocarditis

Yanfei Chen1, Xingzhu Liu2, Lijuan Meng3

  • 1Department of Cardiology, Kunming Children's Hospital, Kunming, Yunnan 650034, China.

Molecular Immunology
|December 3, 2025
PubMed
Abstract

Insights

Annexin 3 (ANXA3) promotes Coxsackievirus B3 (CVB3)-induced viral myocarditis (VMC) by enhancing M1 macrophage polarization. Reducing ANXA3 expression offers a potential therapeutic strategy for VMC treatment.

Area of Science:

  • Immunology
  • Virology
  • Cardiology

Background:

  • Viral myocarditis (VMC) is a pediatric inflammatory heart condition primarily caused by Coxsackievirus B3 (CVB3).
  • M1 macrophage polarization is a critical factor in CVB3-induced myocarditis pathogenesis.
  • Annexin 3 (ANXA3) is implicated in macrophage activation processes.

Purpose of the Study:

  • To investigate the role of ANXA3 in CVB3-induced myocarditis.
  • To explore the function of ANXA3 in macrophage polarization during CVB3 infection.

Main Methods:

  • Established a CVB3-induced myocarditis mouse model and infected RAW264.7 cells.
  • Quantified gene and protein expression using RT-qPCR, western blotting, immunohistochemistry, and ELISA.
  • Assessed cardiac pathology via HE staining and measured myocardial injury markers.

Main Results:

  • ANXA3 expression was elevated in VMC.
  • ANXA3 knockdown attenuated VMC progression, reduced cardiac inflammation, and decreased injury markers.
  • ANXA3 knockdown inhibited M1 macrophage polarization and pro-inflammatory cytokine release (IL-1β, IL-6, TNF-α).
  • CVB3 infection activated the TLR4/MyD88/NF-κB pathway, increasing ANXA3 expression and promoting M1 polarization.

Conclusions:

  • ANXA3 plays a crucial role in promoting CVB3-induced myocarditis.
  • Targeting ANXA3 presents a potential therapeutic avenue for VMC.
Keywords:
ANXA3Coxsackievirus B3Macrophage polarizationNF-κBTLR4/MyD88 pathwayViral myocarditis

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