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[Of note, 2-week hyperhomocysteinemia (HHcy) ApoE(-/-) mice showed accelerated lesion formation and parallel lower Trx expression in macrophages than ApoE(-/-) mice, suggesting that HHcy-induced sustained oxidative stress in vivo might account for impaired Trx and hence increased ROS production and MCP-1 secretion from macrophages, and subsequently accelerated atherogenesis.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
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