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Spontaneous preterm delivery accounts for approximately 8% of all live births worldwide (GBD 2016 Causes of Death Collaborators., 2017), which is the leading cause of perinatal mortality and the second major cause of death in children under 5 years old. Survivals of preterm birth are often faced with shortand long-term morbidity (Slomski, 2021). Adverse environmental exposure and changes in fertility policies may lead to a gradual increase in the premature birth rate (Liu et al.,2019; Deng et al., 2021). Infection-induced inflammation is thought to be the primary cause of rupture of membranes and uterine contraction which consequently results in preterm birth (Kim et al., 2015; Bian et al., 2021; Xu et al., 2021; Xie and Ying, 2020; Pan et al., 2020). However, due to the lack of sufficient understanding of the underlying mechanism, current diagnosis and treatment are often based on clinical symptoms, which sometimes yields inconsistent outcomes. With the emergence of new technologies such as multi-omics analysis (Wang et al., 2022), searching for novel marker genes and signaling pathways related to premature delivery has become a research hotspot (Wang et al., 2018). As a result, a number of novel and pivotal signalers have been revealed, which may be of potential value for the determination of gestational age and prediction of delivery time. Metabolites and humoral factors derived from the fetus per se or fetal appendage appear to be particularly appealing (Chen et al., 2020; Liang et al., 2020; Wang et al., 2018). These findings offer deep insight into the mechanism of preterm birth and expand new visions for the prediction of preterm birth. While uterine contraction inhibitors and antibiotics are important drugs for the treatment of preterm labor (Sharp and Alfirevic, 2014), the effect of hormones on promoting fetal lung maturation in premature infants has been verified over a wider OPEN ACCESS