Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, USA.
Adv Exp Med Biol. 2024;1441:559-571. doi: 10.1007/978-3-031-44087-8_30.
Atrioventricular septal defects (AVSD), also known as a common atrioventricular canal (CAVC), are clinically severe heart malformations that affect about 1 out of every 2100 live births. AVSD makes up about 5% of all congenital heart defects. AVSD is associated with cytogenetic disorders such as Down syndrome and numerous other rare genetic syndromes, but also occurs as a simplex trait. Studies in mouse models have identified over 100 genetic mutations that have the potential to cause an AVSD. However, studies in humans indicate that AVSD is genetically heterogeneous, and that the cause in humans is very rarely a single-gene defect. Familial cases do occur albeit rarely, usually with autosomal dominant inheritance and variable expression. In addition, the frequent occurrence of AVSD in some syndromes with known genetic causes such as heterotaxy syndrome points to additional genes/pathways that increase AVSD risk. Accordingly, while the genetic underpinnings for most AVSD remain unknown, there have been advances in identifying genetic risk factors for AVSD in both syndromic and nonsyndromic cases. This chapter summarizes the current knowledge of the genetic basis for AVSD.
房室间隔缺损(AVSD),也称为常见的房室管(CAVC),是一种严重的临床心脏畸形,影响每 2100 例活产儿中的 1 例。AVSD 约占所有先天性心脏病的 5%。AVSD 与细胞遗传学疾病有关,如唐氏综合征和许多其他罕见的遗传综合征,但也作为单纯性特征发生。在小鼠模型中的研究已经确定了超过 100 种具有导致 AVSD 潜力的基因突变。然而,人类研究表明 AVSD 在遗传上是异质的,并且在人类中,其病因很少是单一基因缺陷。家族病例确实存在,尽管很少见,通常为常染色体显性遗传和可变表达。此外,在一些具有已知遗传原因的综合征中,如异构综合征中经常发生 AVSD,这表明存在增加 AVSD 风险的其他基因/途径。因此,虽然大多数 AVSD 的遗传基础仍不清楚,但在综合征和非综合征病例中,已经在确定 AVSD 的遗传风险因素方面取得了进展。本章总结了 AVSD 遗传基础的现有知识。