STING regulates the transformation of the proinflammatory macrophage phenotype by HIF1A into autoimmune myocarditis

Hua, Xiumeng; Bao, Mengni; Han, Mei; Sun, Zhe; Xu, Mengda; Chen, Xiao; Mo, Xiuxue; Hu, Gang; Tao, Menghao; Song, Jiangping

doi:10.1016/j.intimp.2023.110523

Cited by 9 publications

(4 citation statements)

References 41 publications

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“…19 Mechanistically, STING initiates proinflammatory macrophage differentiation during the acute phase of myocarditis, and macrophages are involved in the pathogenesis of myocarditis via hypoxia-inducible factor-1α (Hif1α). 25 Furthermore, the stimulation of myocardial tissue by pathogens leads to dendritic cell activation, which in turn induces the infiltration of CD4 + T cells into myocardial tissues. This suggests that DCs not only contribute to the initiation of myocarditis but also exacerbate its progression.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, our results found increased macrophage infiltration to be most pronounced in myocarditis, which aligns with prior reports indicating that macrophages constitute the major immune cell population (>60%) in all disease stages of myocarditis . Mechanistically, STING initiates proinflammatory macrophage differentiation during the acute phase of myocarditis, and macrophages are involved in the pathogenesis of myocarditis via hypoxia-inducible factor-1α ( Hif1α ) . Furthermore, the stimulation of myocardial tissue by pathogens leads to dendritic cell activation, which in turn induces the infiltration of CD4 + T cells into myocardial tissues.…”

Section: Discussionmentioning

confidence: 99%

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STING-Targeted PET Imaging for Specific Detection and Therapeutic Monitoring of Myocarditis

Ye,

Lu,

Zhu

et al. 2024

Mol. Pharmaceutics

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

STING-Targeted PET Imaging for Specific Detection and Therapeutic Monitoring of Myocarditis

Ye,

Lu,

Zhu

et al. 2024

Mol. Pharmaceutics

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“…Alternatively though, within the biomedical research space, recent years have witnessed enormous advances in single cell technologies. These single cell technologies, and in particular scRNA-seq, are especially helpful in defining immune cell subpopulations (173), and identification of immune cell subpopulations that are enriched for IFN-related genes has been important to several recent studies elucidating the molecular pathological basis of cardiac diseases (37,102,(174)(175)(176)(177)(178)(179)(180). Fundamental studies exploiting single cell technologies and defining immune cell subpopulations based on IFN-related gene enrichment are likely to continue to advance our understanding of the role of inflammation in heart disease in years ahead.…”

Section: Summary and Future Directionsmentioning

confidence: 99%

Interferons and interferon-related pathways in heart disease

Tran,

Batchu,

Advani

2024

Front. Cardiovasc. Med.

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Interferons (IFNs) and IFN-related pathways play key roles in the defence against microbial infection. However, these processes may also be activated during the pathogenesis of non-infectious diseases, where they may contribute to organ injury, or function in a compensatory manner. In this review, we explore the roles of IFNs and IFN-related pathways in heart disease. We consider the cardiac effects of type I IFNs and IFN-stimulated genes (ISGs); the emerging role of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway; the seemingly paradoxical effects of the type II IFN, IFN-γ; and the varied actions of the interferon regulatory factor (IRF) family of transcription factors. Recombinant IFNs and small molecule inhibitors of mediators of IFN receptor signaling are already employed in the clinic for the treatment of some autoimmune diseases, infections, and cancers. There has also been renewed interest in IFNs and IFN-related pathways because of their involvement in SARS-CoV-2 infection, and because of the relatively recent emergence of cGAS-STING as a pattern recognition receptor-activated pathway. Whether these advances will ultimately result in improvements in the care of those experiencing heart disease remains to be determined.

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“…Nitrofuran derivatives can palmitoylate Cys99 on STING proteins to alter their molecular properties and affect their response-mediated I-IFN transcription [ 123 ]. Hua et al[ 124 ] showed that in α-MyHC-induced autoimmune myocarditis (EAM), consecutive intraperitoneal injection of 1 μmol of C-176 for 14 days results in an inflammatory response in EAM, with IFN-β, TNF-α, CCL2, and F4/80 expression that is ameliorated by blocking macrophage STING expression. In an in vitro study, C-176 blocked the PA-induced NLRP3-mediated endothelial cell pyroptosis and I-IFN transcription.…”

Section: Therapeutic Targets Of the Cgas-sting Pathway In Cvdsmentioning

confidence: 99%

The cGAS-STING pathway in cardiovascular diseases: from basic research to clinical perspectives

An,

Li,

Chen

et al. 2024

Cell Biosci

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The cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase-stimulator of interferon genes (cGAS-STING) signaling pathway, an important component of the innate immune system, is involved in the development of several diseases. Ectopic DNA-induced inflammatory responses are involved in several pathological processes. Repeated damage to tissues and metabolic organelles releases a large number of damage-associated molecular patterns (mitochondrial DNA, nuclear DNA, and exogenous DNA). The DNA fragments released into the cytoplasm are sensed by the sensor cGAS to initiate immune responses through the bridging protein STING. Many recent studies have revealed a regulatory role of the cGAS-STING signaling pathway in cardiovascular diseases (CVDs) such as myocardial infarction, heart failure, atherosclerosis, and aortic dissection/aneurysm. Furthermore, increasing evidence suggests that inhibiting the cGAS-STING signaling pathway can significantly inhibit myocardial hypertrophy and inflammatory cell infiltration. Therefore, this review is intended to identify risk factors for activating the cGAS-STING pathway to reduce risks and to simultaneously further elucidate the biological function of this pathway in the cardiovascular field, as well as its potential as a therapeutic target.

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STING regulates the transformation of the proinflammatory macrophage phenotype by HIF1A into autoimmune myocarditis

Cited by 9 publications

References 41 publications

STING-Targeted PET Imaging for Specific Detection and Therapeutic Monitoring of Myocarditis

STING-Targeted PET Imaging for Specific Detection and Therapeutic Monitoring of Myocarditis

Interferons and interferon-related pathways in heart disease

The cGAS-STING pathway in cardiovascular diseases: from basic research to clinical perspectives

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