Metabolism: a potential regulator of neutrophil fate
Frontiers in Immunology, ISSN: 1664-3224, Vol: 15, Page: 1500676
2024
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
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Review Description
Neutrophils are essential components of the innate immune system that defend against the invading pathogens, such as bacteria, viruses, and fungi, as well as having regulatory roles in various conditions, including tissue repair, cancer immunity, and inflammation modulation. The function of neutrophils is strongly related to their mode of cell death, as different types of cell death involve various cellular and molecular alterations. Apoptosis, a non-inflammatory and programmed type of cell death, is the most common in neutrophils, while other modes of cell death, including NETOsis, necrosis, necroptosis, autophagy, pyroptosis, and ferroptosis, have specific roles in neutrophil function regulation. Immunometabolism refers to energy and substance metabolism in immune cells, and profoundly influences immune cell fate and immune system function. Intercellular and intracellular signal transduction modulate neutrophil metabolism, which can, in turn, alter their activities by influencing various cell signaling pathways. In this review, we compile an extensive body of evidence demonstrating the role of neutrophil metabolism in their various forms of cell death. The review highlights the intricate metabolic characteristics of neutrophils and their interplay with various types of cell death.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85212282349&origin=inward; http://dx.doi.org/10.3389/fimmu.2024.1500676; http://www.ncbi.nlm.nih.gov/pubmed/39697327; https://www.frontiersin.org/articles/10.3389/fimmu.2024.1500676/full; https://dx.doi.org/10.3389/fimmu.2024.1500676; https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1500676/full
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