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The gene ratio of ROS can induce the upregulation of NF-B, thus elevating the expression of vascular endothelial growth factor and other proangiogenic factors to compensate the antanginogenic effect caused by A

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Mechanistically, regardless of ART treatment status, the dysregulation of monocyte subsets and proinflammatory programmes is partially driven by age- and HIV-associated impairments in haematopoietic stem cell differentiation [49, 50]

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