The lifelong impact of fetal growth restriction on cardiac development.
The lifelong impact of fetal growth restriction on cardiac development.
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DOI：
10.1038/s41390-018-0069-x
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发表时间：
2018-10
影响因子：
3.6
通讯作者：
Stansfield BK
中科院分区：
文献类型：
--
作者：
Masoumy EP;Sawyer AA;Sharma S;Patel JA;Gordon PMK;Regnault TRH;Matushewski B;Weintraub NL;Richardson B;Thompson JA;Stansfield BK
母体营养限制（MNR）是胎儿生长受限（FGR）的普遍原因，是心脏病和心血管死亡率的独立预测因子。我们的目的是研究MNR诱导的FGR对心脏结构的发育和长期影响，在一个模型中，密切模仿人类的发展。减少豚鼠母猪从妊娠前到哺乳期的总热量摄入用于诱导FGR。在妊娠晚期胎儿、新生儿和成年豚鼠心脏中评估心肌细胞的增殖、分化和凋亡。对胎儿心脏进行蛋白质组学分析和途径富集。在MNR-FGR胎儿和新生儿心脏中，心肌细胞增殖和单核细胞数量增加，表明心肌细胞分化延迟。在MNR-FGR动物的胎儿心脏中，细胞凋亡显著升高，心肌细胞总数减少，后者在整个新生儿和成年期保持不变。成年MNR-FGR心脏中心肌细胞总数的减少伴随着过度肥大和结构紊乱。通路分析鉴定了与细胞增殖、分化和存活相关的基因。FGR在发育的关键窗口期间影响心肌细胞发育，导致心肌细胞数量的永久性缺乏和啮齿动物模型中的代偿性肥大，该模型重现了人类发育。
Maternal nutrient restriction (MNR) is a widespread cause of fetal growth restriction (FGR), an independent predictor of heart disease and cardiovascular mortality. Our objective was to examine the developmental and long-term impact of MNR-induced FGR on cardiac structure in a model that closely mimics human development. A reduction in total caloric intake spanning pre-gestation through to lactation in guinea pig sows was used to induce FGR. Proliferation, differentiation, and apoptosis of cardiomyocytes were assessed in late-gestation fetal, neonatal, and adult guinea pig hearts. Proteomic analysis and pathway enrichment were performed on fetal hearts. Cardiomyocyte proliferation and number of mononucleated cells was enhanced in the MNR-FGR fetal and neonatal heart, suggesting a delay in cardiomyocyte differentiation. In fetal hearts of MNR-FGR animals, apoptosis was markedly elevated and the total number of cardiomyocytes reduced, the latter remaining so throughout neonatal and into adult life. A reduction in total cardiomyocyte number in adult MNR-FGR hearts was accompanied by exaggerated hypertrophy and a disorganized architecture. Pathway analysis identified genes related to cell proliferation, differentiation, and survival. FGR influences cardiomyocyte development during critical windows of development, leading to a permanent deficiency in cardiomyocyte number and compensatory hypertrophy in a rodent model that recapitulates human development.
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影响因子：
5.5
作者：
Louey, Samantha;Jonker, Sonnet S.;Thornburg, Kent L.
通讯作者：
Thornburg, Kent L.
影响因子：
20.1
作者：
Chen, Xiongwen;Wilson, Rachel M.;Houser, Steven R.
通讯作者：
Houser, Steven R.
DOI：
10.1152/ajpregu.00360.2004
发表时间：
2005-01-01
影响因子：
2.8
作者：
Kind, KL;Roberts, CT;Owens, JA
通讯作者：
Owens, JA
影响因子：
37.8
作者：
Crispi, Fatima;Bijnens, Bart;Gratacos, Eduard
通讯作者：
Gratacos, Eduard
影响因子：
3.9
作者：
ASHWELL, M;PURKINS, L;DAY, KC
通讯作者：
DAY, KC