Roles of IL-33 in the Pathogenesis of Cardiac Disorders

Jiang, Chunjie; Jin, Xuemei; Li, Chunlei; Wen, Luona; Wang, Yuqi; Li, Xiaojian; Zhang, Zhi; Tan, Rongshao

doi:10.1177/15353702231198075

Cited by 2 publications

(1 citation statement)

References 75 publications

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“… 430 , 431 M2 macrophages can secrete factors like oncostatin M and IL‐33 that promote cardiomyocyte proliferation and survival, potentially contributing to new cardiac muscle. 432 , 433 However, excessive inflammation and prolonged M1 macrophage activation can lead to adverse cardiac remodeling and heart failure. 434 , 435 Therefore, modulating macrophage phenotypes and functions may represent a therapeutic strategy for improving cardiac repair and regeneration.…”

Section: Macrophages: Orchestrators Of Tissue Repair and Regenerationmentioning

confidence: 99%

Macrophage plasticity: signaling pathways, tissue repair, and regeneration

Yan,

Wang,

Cai

et al. 2024

MedComm

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Macrophages are versatile immune cells with remarkable plasticity, enabling them to adapt to diverse tissue microenvironments and perform various functions. Traditionally categorized into classically activated (M1) and alternatively activated (M2) phenotypes, recent advances have revealed a spectrum of macrophage activation states that extend beyond this dichotomy. The complex interplay of signaling pathways, transcriptional regulators, and epigenetic modifications orchestrates macrophage polarization, allowing them to respond to various stimuli dynamically. Here, we provide a comprehensive overview of the signaling cascades governing macrophage plasticity, focusing on the roles of Toll‐like receptors, signal transducer and activator of transcription proteins, nuclear receptors, and microRNAs. We also discuss the emerging concepts of macrophage metabolic reprogramming and trained immunity, contributing to their functional adaptability. Macrophage plasticity plays a pivotal role in tissue repair and regeneration, with macrophages coordinating inflammation, angiogenesis, and matrix remodeling to restore tissue homeostasis. By harnessing the potential of macrophage plasticity, novel therapeutic strategies targeting macrophage polarization could be developed for various diseases, including chronic wounds, fibrotic disorders, and inflammatory conditions. Ultimately, a deeper understanding of the molecular mechanisms underpinning macrophage plasticity will pave the way for innovative regenerative medicine and tissue engineering approaches.

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Section: Macrophages: Orchestrators Of Tissue Repair and Regenerationmentioning

confidence: 99%

Macrophage plasticity: signaling pathways, tissue repair, and regeneration

Yan,

Wang,

Cai

et al. 2024

MedComm

View full text Add to dashboard Cite

show abstract

FBXL19 in endothelial cells protects the heart from influenza A infection by enhancing antiviral immunity and reducing cellular senescence programs

Xia,

Chen,

Taleb

et al. 2024

American Journal of Physiology-Heart and Circulatory Physiology

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Influenza A virus (IAV) infection while primarily affects the lungs, it is often associated with cardiovascular complications. However, the mechanisms underlying this association are not fully understood. Here, we investigated the potential role of FBXL19, a member of the Skp1-Cullin-F-box family of E3 ubiquitin ligase, in IAV-induced cardiac inflammation. We demonstrated that FBXL19 overexpression in endothelial cells (ECs) reduced viral titers and IAV matrix protein 1 (M1) levels, while increasing antiviral genes expression, including interferon (IFN)-α, β, γ and RANTES in the cardiac tissue of IAV-infected mice. Moreover, EC-specific overexpression of FBXL19 attenuated the IAV infection-reduced interferon regulatory factor 3 (IRF3) level without altering its mRNA level, and suppressed cardiac inflammation. Furthermore, IAV infection triggered cellular senescence programs in the heart as indicated by the upregulation of p16 and p21 mRNA levels, and the downregulation of lamin B1 levels, which were partially reversed by FBXL19 overexpression in ECs. Our findings indicate that EC-specific overexpression of FBXL19 protects against IAV-induced cardiac damage by enhancing interferon-mediated antiviral signaling, reducing cardiac inflammation, and suppressing cellular senescence programs.

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Roles of IL-33 in the Pathogenesis of Cardiac Disorders

Cited by 2 publications

References 75 publications

Macrophage plasticity: signaling pathways, tissue repair, and regeneration

Macrophage plasticity: signaling pathways, tissue repair, and regeneration

FBXL19 in endothelial cells protects the heart from influenza A infection by enhancing antiviral immunity and reducing cellular senescence programs

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