Abstract
Preeclampsia (PE) is a common pregnancy-related complication, and polymorphisms in angiotensinogen (AGT), angiotensin-converting enzyme (ACE), and angiotensin II type 1 receptor (AT1R) are believed to contribute to PE development. We implemented a hybrid study to investigate the influence of maternal and fetal ACE I/D, ACE G2350A, AGT M235T, AGT T174M, and AT1R A1166C polymorphisms on PE in Han Chinese women. Polymorphisms were genotyped in 1,488 subjects (256 patients experiencing PE, along with their fetuses and partners, and 360 normotensive controls with their fetuses). Transmission disequilibrium tests revealed that ACE I/D (P = 0.041), ACE G2350A (P = 0.035), and AT1R A1166C (P = 0.018) were associated with maternal PE. The log-linear analyses revealed that mothers whose offspring carried the MM genotype of AGT M235T had a higher risk of PE (OR = 1.54, P = 0.010), whereas mothers whose offspring carried the II genotype of ACE I/D or the GG genotype of ACE G2350A had a reduced risk (OR = 0.58, P = 0.039; OR = 0.47, P = 0.045, respectively). Our findings demonstrate that fetal ACE I/D, ACE G2350A, AGT M235T, and AT1R A1166C polymorphisms may play significant roles in PE development among pregnant Han Chinese women.
Highlights
The renin-angiotensin system (RAS) is a peptide cascade comprising the following proteins: rennin (REN), angiotensinogen (AGT), angiotensin-converting enzyme (ACE), and angiotensin I, II (ANG I, ANG II), and 1–7 (ANG1–7), as well as angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R); RAS is believed to contribute to PE development[7,8,9]
The average fetal birth weight was lower in patients than in controls (2.97 ± 0.68 kg vs. 3.27 ± 0.44 kg, P < 0.001), and the PE group had a higher proportion of intrauterine growth restriction (IUGR) cases than the control group (27.5% vs. 3.9%, P < 0.001)
This is the first study to investigate the association between maternal/fetal RAS polymorphisms and PE in a hybrid design with a large sample size of 1,488 patients, focusing on the Chinese Han population
Summary
The renin-angiotensin system (RAS) is a peptide cascade comprising the following proteins: rennin (REN), angiotensinogen (AGT), angiotensin-converting enzyme (ACE), and angiotensin I, II (ANG I, ANG II), and 1–7 (ANG1–7), as well as angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R); RAS is believed to contribute to PE development[7,8,9]. In addition to circulating RAS, a tissue-based RAS exists in the utero-placental unit[7]. This local RAS influences the regulation of regional maternal intervillous blood flow and assists in local spiral artery remodeling, and its dysregulation causes shallow placental implantation and utero-placental ischemia[12, 13], leading to PE14. Retrospective studies have suggested that heritable allelic variations, those in the utero-placental RAS, are associated with defective placental vascular development. Analysis of these variations could become the cornerstone for understanding the genetics of PE15. The objective of the current study was to investigate the effects of these maternal and fetal polymorphisms, as well as potential maternal gene–environment interactions, on PE
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