动脉导管未闭（PDA）是新生儿动脉导管在出生后保持持续开放状态的一种先天性心脏病。PDA在新生儿尤 其是早产儿中发病率高，如未及时治疗，往往会导致严重并发症，增加早产儿病死率。目前治疗PDA的药物主要是通过 COX酶抑制剂阻断前列腺素的产生使动脉导管关闭，但有一定局限性和不良反应。研究影响动脉导管关闭的分子机制， 理解PDA发病机制，有助于研发促进PDA关闭的新型药物，以减少药物治疗的失败率和不良反应。本文综述影响动脉导 管闭合的分子机制。

Patent ductus arteriosus (PDA) is a congenital heart disease in which the ductus arteriosus of newborns remains open continuously after birth. The incidence of PDA in newborns, especially premature infants, is very high. If it is not treated in time, it will often cause serious complications and increase the mortality of premature infants. At present, non-selective COX enzyme inhibitors were the main drugs used to treat PDA to close the ductus arteriosus by blocking the production of prostaglandin, which have certain limitations and side effects. Studying the molecular mechanisms that affect the closure of ductus arteriosus and understanding the pathogenesis of PDA will help develop new targeted drugs that promote ductus arteriosus closure in PDA patients to reduce the failure rate and side effects of drug therapy. This article summarizes the studies on molecular mechanisms affecting the closure of ductus arteriosus, expounds the possible pathogenesis of PDA, and provides new insights for exploring new treatment methods