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To complement these findings, we tested whether agonists of the candidate channels could restore NET formation in XKR8-deficient cells
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Considering mitochondrial dysfunction is a well-established biological hallmark of aging [96] and dysfunctional mitochondria are directly implicated in vascular aging [47] , it is warranted to investigate the role of increased glycolytic flux as a mechanism mediating cellular senescence-induced vascular aging
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