Abstract:

Protein lactylation modification mediated by lactate accumulation is a new type of epigenetic modification. It is a protein modification method in which lactyl groups are covalently coupled to lysine residues of proteins to regulate gene expression. Due to the physiological hypoxia in the placenta during early pregnancy, placental cells have developed a series of hypoxia-response mechanisms. Different degrees of protein lactylation modification have been found to be involved in these mechanisms. Protein lactylation modification mediates cellular energy flow, trophoblast cell function expression, immune function, and inflammatory responses. When pathological hypoxia occurs in the placenta, it can lead to placental dysfunction, abnormal trophoblast cell proliferation, and impaired invasion function. On this basis, pregnancy complications such as preeclampsia (PE), gestational diabetes mellitus (GDM), and recurrent spontaneous abortion (RSA) may occur. High levels of protein lactylation in patients with PE and GDM can cause placental dysfunction, reduce the migration and invasion ability of trophoblast cells, and participate in the occurrence and development of the diseases. Protein lactylation modification participates in the pathogenesis of RSA by regulating trophoblast cell apoptosis and the immune function at the maternal-fetal interface. This review summarizes the research progress of protein lactylation modification in placental hypoxia and pregnancy complications, aiming to provide new ideas for the prevention and treatment of placental-derived pregnancy complications related to fetal hypoxia.

Key words: Protein processing, post-translational, Placenta, Hypoxia, Pregnancy complications, Lactylation