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In murine models, short-term exposure to low-dose LPS induces long-lasting monocyte polarization toward a proinflammatory phenotype, aggravating atherosclerotic lesion development (100)

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The molecular basis of this multi-metal cooperation appears to lie in the simultaneous activation of several stress-response pathways that each have distinct metal requirements but converge on a common goal: thwarting apoptosis and repairing drug-induced damage