ArticleBasic research in cardiology2025
The cGAS-STING pathway promotes acute ischemia-induced neutropoiesis and neutrophil priming in the bone marrow.
Article in Basic research in cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Emerging roles of the cGAS/STING pathway in cardiovascular diseases.The Journal of clinical investigation · 2026Review
- Trained Immunity in Neutrophils and Mononuclear Phagocytes: Mechanisms and Pathophysiological Functions.Cells · 2026Review
- Interactions between neutrophil extracellular traps and macrophages: the key to inflammatory diseases.Frontiers in immunology · 2026Review
- Neutrophil Heterogeneity after Myocardial Infarction.Journal of innate immunity · 2026Review
- Activation of cGAS-STING Pathway by DAI-Triggered Ferroptosis in CRC Cells Reprograms TAMs Balance to Promote Anti-Tumor Immunity.Cancer science · 2025Article
- Dynamic STING repression orchestrates immune cell development and function.Science immunology · 2025Article
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8 authors.
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Abstract
Our previous work demonstrated that the DNA-sensing receptor cyclic GMP-AMP synthase (cGAS) negatively affects post-infarct repair by promoting pro-inflammatory macrophages. However, whether cGAS and its downstream partner STING (Stimulator of Interferon Genes) regulate neutrophil production and function in the context of acute myocardial ischemia remains unclear. This study investigated the role of the cGAS-STING pathway in neutropoiesis (neutrophil production and differentiation) and examined whether ischemia primes neutrophils in the bone marrow via this pathway, enhancing their functionality and contributing to cardiac inflammatory injury. Using myocardial infarction (MI) models in wild-type (WT), Cgas
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