The DOI matches its Crossref record; 139 of the 139 references it cites were found in a registry or an index.
The role of inflammation in the pathology of preeclampsia
Open accessAbstract
Preeclampsia (PE) affects 5–7% of all pregnancies in the United States and is the leading cause of maternal and prenatal morbidity. PE is associated with hypertension after week 20 of gestation, decreased renal function and small-for-gestational-age babies. Women with PE exhibit chronic inflammation and production of autoantibodies. It is hypothesized that during PE, placental ischaemia occurs as a result of shallow trophoblast invasion which is associated with an immune imbalance where pro-inflammatory CD4+ T-cells are increased and T regulatory cells (Tregs) are decreased. This imbalance leads to chronic inflammation characterized by oxidative stress, pro-inflammatory cytokines and autoantibodies. Studies conducted in our laboratory have demonstrated the importance of this immune imbalance in causing hypertension in response to placental ischaemia in pregnant rats. These studies confirm that increased CD4+ T-cells and decreased Tregs during pregnancy leads to elevated inflammatory cytokines, endothelin (ET-1), reactive oxygen species (ROS) and agonistic autoantibodies to the angiotensin II (Ang II), type 1 receptor (AT1-AA). All of these factors taken together play an important role in increasing the blood pressure during pregnancy. Specifically, this review focuses on the decrease in Tregs, and their associated regulatory cytokine interleukin (IL)-10, which is seen in response to placental ischaemia during pregnancy. This study will also examine the effect of regulatory immune cell repopulation on the pathophysiology of PE. These studies show that restoring the balance of the immune system through increasing Tregs, either by adoptive transfer or by infusing IL-10, reduces the blood pressure and pathophysiology associated with placental ischaemia in pregnant rats.
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Cites
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Cited by
Preston, E. V., Hivert, M.-F., Fleisch, A. F., Calafat, A. M., Sagiv, S. K., Perng, W., Rifas-Shiman, S. L., Chavarro, J. E., Oken, E., Zota, A. R., et al. (2022) · Environment International · doi:10.1016/j.envint.2022.107335 · Cited by 78
Dargaud, Y., Rugeri, L., Fleury, C., Battie, C., Gaucherand, P., Huissoud, C., Rudigoz, R. C., Desmurs‐Clavel, H., Ninet, J., & Trzeciak, M. C. (2017) · Journal of Thrombosis and Haemostasis · doi:10.1111/jth.13660 · Cited by 44
Risk for preeclampsia following exposure to PM2.5 during pregnancy
Daniel, S., Kloog, I., Factor-Litvak, P., Levy, A., Lunenfeld, E., & Kioumourtzoglou, M.-A. (2021) · Environment International · doi:10.1016/j.envint.2021.106636 · Cited by 26
Rowe, C. W., Rosee, P., Sathiakumar, A., Ramesh, S., Qiao, V., Huynh, J., Dennien, G., Weaver, N., & Wynne, K. (2024) · Diabetic Medicine · doi:10.1111/dme.15262 · Cited by 6
Kiolbasa, M., Kotlarz, A., Kaminiów, K., & Pastuszczak, M. (2025) · International Journal of STD & AIDS · doi:10.1177/09564624241303816 · Cited by 2
Metadata
- Authors
- Harmon, A. C., Cornelius, D. C., Amaral, L. M., Faulkner, J. L., Cunningham, M. W., Wallace, K., & LaMarca, B.
- Venue
- Clinical Science
- Publisher
- Portland Press Ltd.
- Published
- 2016-02-04
- Volume
- 130
- Issue
- 6
- Pages
- 409-419
- ISSN
- 0143-5221 (ISSN-L)
- 1470-8736
- OpenAlex
- W2290324068
- Cited by
- 565
- References
- 139
- FWCI
- 40.76
- Type
- journal article
- Language
- en
- Open access
- green
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