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Iron-dependent apoptosis causes embryotoxicity in inflamed and obese pregnancy

AL. Fisher, V. Sangkhae, K. Balušíková, NJ. Palaskas, T. Ganz, E. Nemeth

. 2021 ; 12 (1) : 4026. [pub] 20210629

Jazyk angličtina Země Velká Británie

Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc21025519

Grantová podpora
R01 HD096863 NICHD NIH HHS - United States
T32 GM065823 NIGMS NIH HHS - United States
UL1 TR000124 NCATS NIH HHS - United States
F31 HD097931 NICHD NIH HHS - United States
UL1 TR001881 NCATS NIH HHS - United States

Iron is essential for a healthy pregnancy, and iron supplementation is nearly universally recommended, regardless of maternal iron status. A signal of potential harm is the U-shaped association between maternal ferritin, a marker of iron stores, and risk of adverse pregnancy outcomes. However, ferritin is also induced by inflammation and may overestimate iron stores during inflammation or infection. In this study, we use mouse models to determine whether maternal iron loading, inflammation, or their interaction cause poor pregnancy outcomes. Only maternal exposure to both iron excess and inflammation, but not either condition alone, causes embryo malformations and demise. Maternal iron excess potentiates embryo injury during both LPS-induced acute inflammation and obesity-induced chronic mild inflammation. The adverse interaction depends on TNFα signaling, causes apoptosis of placental and embryo endothelium, and is prevented by anti-TNFα or antioxidant treatment. Our findings raise important questions about the safety of indiscriminate iron supplementation during pregnancy.

Citace poskytuje Crossref.org

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