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Determining the signaling pathways and molecular players that regulate NET release is therefore critical, not only for advancing our understanding of neutrophil biology but also for identifying new therapeutic targets to treat disorders associated with aberrant NETosis

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In order to elucidate such mechanisms, the aim of this work was to study, in mice with partial IGF-1 deficiency, liver expression of genes involved in glucose and lipid metabolism as well as serum levels of glucose, triglycerides and cholesterol, as well as liver malondialdehyde (MDA) levels, as a marker for oxidative damage

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