ArticleThe Journal of physiology2005
Intra-uterine growth restriction and the programming of left ventricular remodelling in female rats.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 51 citations in OpenAlex.
- Fetal Cardiac Lipid Sensing Triggers an Early and Sex-related Metabolic Energy Switch in Intrauterine Growth Restriction.The Journal of clinical endocrinology and metabolism · 2021Article
- Maternal Fructose Intake Exacerbates Cardiac Remodeling in Offspring with Ventricular Pressure Overload.Nutrients · 2021Article
- Neonatal Growth Restriction Slows Cardiomyocyte Development and Reduces Adult Heart Size.Anatomical record (Hoboken, N.J. : 2007) · 2018Article
- Cardiac Development and Transcription Factors: Insulin Signalling, Insulin Resistance, and Intrauterine Nutritional Programming of Cardiovascular Disease.Journal of nutrition and metabolism · 2018Review
- Long term effects of fetal undernutrition on rat heart. Role of hypertension and oxidative stress.PloS one · 2017Article
- IGF-2R-Gαq signaling and cardiac hypertrophy in the low-birth-weight lamb.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- The influence of hypoxia during different pregnancy stages on cardiac collagen accumulation in the adult offspring.BioMed research international · 2014Article
- Coenzyme Q10 prevents accelerated cardiac aging in a rat model of poor maternal nutrition and accelerated postnatal growth.Molecular metabolism · 2013Article
- The effect of feto-maternal size and childhood growth on left ventricular mass and arterial stiffness in Afro-Caribbean children.Journal of human hypertension · 2011Article
- Developmental programming resulting from maternal obesity in mice: effects on myocardial ischaemia-reperfusion injury.Experimental physiology · 2009Article
- Maternal dietary supplementation with saturated, but not monounsaturated or polyunsaturated fatty acids, leads to tissue-specific inhibition of offspring Na+,K+-ATPase.The Journal of physiology · 2008Article
- Role of fetal programming in the development of hypertension.Future cardiology · 2008Article
- Maternal nutrient restriction and the fetal left ventricle: decreased angiotensin receptor expression.Reproductive biology and endocrinology : RB&E · 2005Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological studies link intra-uterine growth restriction (IUGR) with increased incidence of hypertension and cardiac disease in adulthood. Our rat model of IUGR supports this contention and provides evidence for the programming of susceptibility for hypertension in all offspring. Moreover, in the female offspring only, gross anatomical changes (cardiac ventricle to body ratios) and increased left cardiac ventricular atrial natriuretic peptide (ANP) mRNA levels provide evidence for programming of cardiac disease in this gender. The aim of the current study was to measure changes in cardiac tissue that support remodelling that could be implicated in the initiation of hypertrophy. Adult female rats from our IUGR model and age- and sex-matched controls were killed at 12 weeks of age. Left cardiac ventricles were removed and used for monitoring changes in several key genes, Na+,K+-ATPase beta1 protein expression, cardiomyocyte morphology and contractility as well as citrate synthase and aconitase activities. When compared to controls, female offspring of our IUGR rat model exhibit higher expression (mRNA) of ANP and the atrial isoform of the myosin light chain, lower levels of Na+,K+-ATPase beta1 protein, increased cardiomyocyte depth and volume, increased sarcomere length, diminished cardiomyocyte contractility and lower aconitase activity. Female offspring of our IUGR rat model exhibit changes as adults that are consistent with the onset of cardiac remodelling. The decrease in aconitase activity suggests that oxidative stress may be implicated in this response.
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