Abstract
Autophagy exists widely in eukaryotic cells and is regulated by a variety of molecular mechanisms. Its physiological functions include providing energy, maintaining cell homeostasis, and promoting apoptosis of abnormal cells. At present, the regulation of autophagy in tumor, degenerative disease, and cardiovascular disease has attracted much attention. Gradually, the role of autophagy in pregnancy tends to be valued. The previous literature has shown that autophagy can influence the occurrence and maintenance of pregnancy from three aspects: embryo (affecting the process of fertilization and embryonic development and the function of trophoblast cells), maternal (decidualization), and maternal-to-fetal immune crosstalk. Undoubtedly, abnormalities in autophagy levels are associated with a variety of pregnancy complications, such as preeclampsia, fetal growth restriction, and preterm delivery which have been proven by human, animal, and in vitro experiments. The regulation of autophagy is expected to be a target for the treatment of these pregnancy complications. This article reviews the research on autophagy, especially about its physiological and pathological regulation during pregnancy.
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Special thanks are also extended to colleagues at the First Affiliated Hospital of Heilongjiang University of Chinese Medicine and Zhejiang Chinese Medical University.
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This research was funded by the National Natural Fund Project (Grant No. 81973894) the Project of General Undergraduate University Youth Innovation Talents by Education Department of Heilongjiang Province (Grant No. UNPYSCT-2018227), and Ph.D. innovation fund (Grant No. 2018bs07).
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XZ, YJ, TJ, and XH wrote the manuscript. YW, LC, and FX took charge of the examination and modification of articles. XZ, YW, and LC revised the manuscript.
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Zhao, X., Jiang, Y., Jiang, T. et al. Physiological and pathological regulation of autophagy in pregnancy. Arch Gynecol Obstet 302, 293–303 (2020). https://doi.org/10.1007/s00404-020-05607-1
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DOI: https://doi.org/10.1007/s00404-020-05607-1