The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Review: The Placenta is a Programming Agent for Cardiovascular Disease
Open accessAbstract
Cardiovascular disease remains the number one killer in western nations in spite of declines in death rates following improvements in clinical care. It has been 20 years since David Barker and colleagues showed that slow rates of prenatal growth predict mortality from ischemic heart disease. Thus, fetal undergrowth and its associated cardiovascular diseases must be due, in part, to placental inadequacies. This conclusion is supported by a number of studies linking placental characteristics with various adult diseases. A “U” shaped relationship between placental-to-fetal weight ratio and heart disease provides powerful evidence that placental growth-regulating processes initiate vulnerabilities for later heart disease in offspring. Recent evidence from Finland indicates that placental morphological characteristics predict risks for coronary artery disease, heart failure, hypertension and several cancers. The level of risk imparted by placental shape is sex dependent. Further, maternal diet and body composition strongly influence placental growth, levels of inflammation, nutrient transport capacity and oxidative stress, with subsequent effects on offspring health. Several animal models have demonstrated the placental roots of vulnerability for heart disease. These include findings that abnormal endothelial development in the placenta is associated with undergrown myocardial walls in the embryo, and that placental insufficiency leads to depressed maturation and proliferation of working cadiomyocytes in the fetal heart. Together these models suggest that the ultimate fitness of the heart is determined by hemodynamic, growth factor, and oxygen/nutrient cues before birth, all of which are influenced, if not regulated by the placenta.
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Citations
Cites
Obesity in Pregnancy Stimulates Macrophage Accumulation and Inflammation in the Placenta
Challier, J. C., Basu, S., Bintein, T., Minium, J., Hotmire, K., Catalano, P. M., & Hauguel-de Mouzon, S. (2008) · Placenta · doi:10.1016/j.placenta.2007.12.010 · Cited by 712 · cited 2×
“Obese women have elevated placental inflammatory cytokine expression [40] and nitrative stress [41] which can impact placental nutrient transport.”
BackgroundForsen, T., Eriksson, J. G., Tuomilehto, J., Osmond, C., & Barker, D. J. P. (1999) · BMJ · doi:10.1136/bmj.319.7222.1403 · Cited by 481
Early onset of coronary artery disease after prenatal exposure to the Dutch famine
Painter, R. C., de Rooij, S. R., Bossuyt, P. M., Simmers, T. A., Osmond, C., Barker, D. J., Bleker, O. P., & Roseboom, T. J. (2006) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/84.2.322 · Cited by 392
Martyn, C., Barker, D., & Osmond, C. (1996) · The Lancet · doi:10.1016/s0140-6736(96)04257-2 · Cited by 381
Effect of placental embolization on the umbilical arterial velocity waveform in fetal sheep
Morrow, R. J., Adamson, S. L., Bull, S. B., & Knox Ritchie, J. W. (1989) · American Journal of Obstetrics and Gynecology · doi:10.1016/0002-9378(89)90783-7 · Cited by 243
The surface area of the placenta and hypertension in the offspring in later life
Barker, D. J. P., Thornburg, K. L., Osmond, C., Kajantie, E., & Eriksson, J. G. (2010) · The International Journal of Developmental Biology · doi:10.1387/ijdb.082760db · Cited by 212
Self-citationJones, H. N., Jansson, T., & Powell, T. L. (2009) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00195.2009 · Cited by 168 · cited 2×
“Furthermore, nutrient transporters have been shown to be responsive to inflammatory cytokines in several tissues, including the placenta [47,48] and thus a pro-inflammatory state, as associated with maternal obesity is a potential contributing factor to modified nutrient transport in the placenta.”
BackgroundPlacental mTOR links maternal nutrient availability to fetal growth
Roos, S., Powell, T. L., & Jansson, T. (2009) · Biochemical Society Transactions · doi:10.1042/bst0370295 · Cited by 156
Louey, S., Jonker, S. S., Giraud, G. D., & Thornburg, K. L. (2007) · The Journal of Physiology · doi:10.1113/jphysiol.2006.122200 · Cited by 116
Self-citation
Cited by
Khong, T. Y., Mooney, E. E., Ariel, I., Balmus, N. C. M., Boyd, T. K., Brundler, M.-A., Derricott, H., Evans, M. J., Faye-Petersen, O. M., Gillan, J. E., et al. (2016) · Archives of Pathology & Laboratory Medicine · doi:10.5858/arpa.2015-0225-cc · Cited by 1,737
Kalogeris, T., Baines, C. P., Krenz, M., & Korthuis, R. J. (2016) · Comprehensive Physiology · doi:10.1002/cphy.c160006 · Cited by 718
Placental Origins of Chronic Disease
Burton, G. J., Fowden, A. L., & Thornburg, K. L. (2016) · Physiological Reviews · doi:10.1152/physrev.00029.2015 · Cited by 717
Self-citationBlake, B. E., & Fenton, S. E. (2020) · Toxicology · doi:10.1016/j.tox.2020.152565 · Cited by 499
Gabory, A., Roseboom, T. J., Moore, T., Moore, L. G., & Junien, C. (2013) · Biology of Sex Differences · doi:10.1186/2042-6410-4-5 · Cited by 344
Metadata
- Authors
- Thornburg, K. L., O'Tierney, P. F., & Louey, S.
- Venue
- Placenta
- Publisher
- Elsevier BV
- Published
- 2010-03
- Volume
- 31
- Pages
- S54-S59
- ISSN
- 0143-4004 (ISSN-L)
- OpenAlex
- W1975184295
- Cited by
- 252
- References
- 9
- FWCI
- 17.38
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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