Department of Pediatrics, University of Utah, UT, United States.
Reprod Toxicol. 2011 Dec;32(4):484-9. doi: 10.1016/j.reprotox.2011.09.004. Epub 2011 Sep 24.
Several epidemiological investigations have shown an association between congenital heart defects and the selective serotonin reuptake inhibitor (SSRI) class of antidepressants. At first glance this association may not seem to make biological sense, especially since, in many cases, serotonin is thought of as a neurotransmitter involved in signaling between neurons. However, serotonin also acts as a signaling molecule during embryogenesis affecting cell proliferation, migration, death, and differentiation. Serotonin may be particularly important for heart development and evidence suggests that from the time that progenitor heart cells are patterned during the establishment of laterality, to formation of the outflow tract, to myocardial cell differentiation, to septation of the heart chambers, the neurotransmitter may act as an important signaling molecule. Thus, numerous investigations have identified potential target sites where serotonin could regulate key cellular processes in cardiac development, thereby providing biological plausibility for the origin of heart defects caused by SSRIs.
几项流行病学调查表明，先天性心脏缺陷与选择性 5-羟色胺再摄取抑制剂（SSRIs）类抗抑郁药之间存在关联。乍一看，这种关联似乎没有生物学意义，尤其是因为在许多情况下，人们认为 5-羟色胺是一种参与神经元之间信号传递的神经递质。然而，5-羟色胺在胚胎发生过程中也作为一种信号分子发挥作用，影响细胞增殖、迁移、死亡和分化。5-羟色胺可能对心脏发育特别重要，有证据表明，从左右定位过程中祖细胞分化，到流出道形成，到心肌细胞分化，再到心腔分隔，神经递质可能作为一种重要的信号分子发挥作用。因此，许多研究已经确定了潜在的靶位，在这些靶位中，5-羟色胺可以调节心脏发育过程中的关键细胞过程，从而为 SSRIs 引起的心脏缺陷的起源提供了生物学上的合理性。
