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Regulatory role of JMJD6 in placental development

Published online by Cambridge University Press:  19 September 2022

Xiaoli Shen*
Affiliation:
Chongqing Reproductive and Genetics Institute, Chongqing Health Center for Women and Children; Women and Children's Hospital of Chongqing Medical University, Chongqing, PR China
Christian De Geyter
Affiliation:
Reproductive Medicine and Gynecological Endocrinology (RME), University Hospital, University of Basel, Basel, Switzerland
Hong Zhang
Affiliation:
Department of Biomedicine, University Hospital, University of Basel, Basel, Switzerland
Guoning Huang
Affiliation:
Chongqing Reproductive and Genetics Institute, Chongqing Health Center for Women and Children; Women and Children's Hospital of Chongqing Medical University, Chongqing, PR China
*
Author for correspondence: Xiaoli Shen, E-mail: [email protected]

Abstract

Correct placental development and function are critical to both the mother's and the foetus' health during pregnancy. Placental function depends on the correct development of the vascular network, which requires proper angiogenesis. Impaired angiogenesis in the placenta can induce foetal growth restriction, preeclampsia, and even foetal death. Placental angiogenesis is finely controlled by ubiquitous and pregnancy-specific angiogenic factors. Jumonji domain-containing protein 6 (JMJD6) is a Fe (II)- and 2-oxoglutarate (2OG)-dependent oxygenase that catalyses arginine demethylation and lysine hydroxylation of histone and non-histone peptides. JMJD6 has been implicated in embryonic development, cellular proliferation and migration, self-tolerance induction in the thymus, and adipocyte differentiation. In this review we present JMJD6's structure and activity, as well as its role in angiogenesis, oxygen sensing, and adverse pregnancy outcomes related to placental development. Understanding the interaction between JMJD6 and other placental factors may identify potential therapeutic targets for correcting abnormal placental angiogenesis and function.

Type
Short Review
Copyright
Copyright © The Author(s), 2022. Published by Cambridge University Press

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