花生四烯酸介导炎症相关心肌纤维化研究进展

Effect of Arachidonic Acid Metabolism on Cardiac Fibrosis Associated with Inflammation

心脏左室纤维化进展作为心脏功能不利因素目前逐渐受到心脏科医生关注。大量研究证据表明,炎症细胞的浸润是心肌纤维化进程中的关键步骤。炎症细胞可以释放花生四烯酸并使其在环氧化酶、脂氧化酶或细胞色素P450表氧化酶等催化物作用下生成具有生物活性的产物,如前列腺素、白三烯、环氧花生四烯酸以及羟基花生四烯酸。这些产物中部分具有促纤维化作用,并参与炎症细胞介导的心肌纤维化通路。现将对目前心肌纤维化通路研究做一综述。

An increase in left ventricular fibrosis is a detrimental process that adversely ＇affects heart function. Strong evidence shows that the infiltration of inflammatory cells is a critical part of the processthatthat results in cardiac fibrosis. Inflammatory cells can release arachidonic acid, which may be further metabolized by cyclooxygenase, lipoxygenase, and cytochrome P450 monooxygenase enzymes to bio- logically active products, including PGs, leukotrienes, epoxyeicosatrienoic acids, and hydroxyeicosatetraenoic acids. Some of these products have profibrotic properties and may represent a pathway by which inflammatory cells initiate and mediate the development of cardiac fibrosis. We review the current literature on the potential link between this path way and cardiac fibrosis.