Metabolism of ADMA, a novel risk factor of cardiovascular diseases and its pathophysiological role

我们研究了不对称二甲基精氨酸（ADMA）在血细胞中的代谢途径，以阐明血浆ADMA升高的调控机制，这是心血管疾病的一个新的危险因素。我们首次发现ADMA在红细胞中被PRMT1和DDAH1积极代谢，并鉴定出含有ADMA残基并与PRMT1相互作用的过氧化氢酶。这些发现表明过氧化氢酶是红细胞中PRMT1甲基化的潜在靶标，可能是血浆ADMA的来源。

We investigated the metabolic pathways of asymmetric dimethylarginine (ADMA) in blood cells to elucidate the regulatory mechanism of elevation of plasma ADMA, a novel risk factor of cardiovascular diseases. We found for the first time that ADMA was actively metabolized by PRMT1 and DDAH1 in erythrocytes and identified catalase that contains ADMA residue and interacts with PRMT1. These findings suggest that catalase is a potential target for methylation by PRMT1 in erythrocytes and may be a source of plasma ADMA.