Preterm birth remains to be one of the most prevalent obstetric complications worldwide. Since there are multiple etiological factors associated with this disease process, an integrative literature search in PubMed and Scopus databases on possible mechanism of action and effect of bisphenols on exposure on human or animal placental samples in preterm birth was conducted. From 2332 articles on initial literature search, 63 studies were included for full data extraction. Altogether, several pathways were shown to be possibly affected by bisphenols, leading to dysregulations in structural and endocrine foundation in the placenta, potential induction of senescence and failure of decidualization in the decidua, and possible propagation of inflammation in the fetal membranes. Combined, these actions may eventually counteract bisphenol-induced relaxation of the myometrium and promote contractility alongside fetal membrane weakening. In totality, these individual impairments in gestation-critical processes may lead to failure of maintenance of pregnancy, and thus effecting preterm birth.
Preeclampsia is one of the major hypertensive diseases of pregnancy. Genetic factors contribute to abnormal placentation. The inadequate transformation of cytotrophoblasts causes failure of maternal spiral arteries’ remodeling and results in narrow, atherotic-prone vessels, leading to relative placental ischemia. This study aims to explore the possibility of identifying dysregulated gene networks that may offer a potential target in the possible prevention of preeclampsia. We performed a weighted gene correlated network analysis (WGCNA) on a subset of gene expression profiles of placental tissues from severe preeclamptic pregnancies. We identified a gene module (number of genes = 402, GS = 0.35, p = 0.02) enriched for several G-protein-coupled receptor (GPCR)-related genes with significant protein–protein molecular interaction (number of genes = 38, FDR = 0.0007) that may play key roles in preeclampsia. Some genes are noted to play key roles in preeclampsia, including LPAR4/5, CRLR, NPY, TACR1/2, and SFRP4/5, whose functions generally relate to angiogenesis and vasodilation or vasoconstriction. Other upregulated genes, including olfactory and orexigenic genes, serve limited functions in the disease pathogenesis. Altogether, this study shows the utility of WGCNA in exploring possible new gene targets, and additionally reinforces the feasibility of targeting GPCRs that may offer intervention against development and disease progression among severe preeclampsia patients.
Preterm birth remains a problem globally, as multiple factors contribute to its etiology and pathogenesis. One such factor is the exposure to environmental toxicants, in which recent literature has described contributory roles in disease progression. This study aims to show research trends and collaborations in papers related to environmental toxicants and preterm birth through a bibliometric analysis to determine hot spots for research as well as to identify already established themes that can point to policy making and development. Using the Scopus database, we were able to identify 956 original research articles from 72 countries between 1955 and 2021; bibliographic information was exported, analyzed, and visualized using Bibliometrix and VOSviewer. There was an annual growth of research and reporting in this area, which significantly increased within the last two decades. The top countries that have published on this topic include the USA (n = 343), China (n = 103), and Australia (n = 43), with strong international collaboration in reports from China. Top journals for publication include Environmental Research (n = 53), Environmental Health Perspectives (n = 47), and Environment International (n = 46). Previous literature focused on establishing toxicants that are significantly associated with preterm birth, with current research focusing on molecular mechanisms of environmental toxicants. Overall, our bibliometric analysis gives a scoping view of the existing research landscape in terms of environmental health and preterm birth.
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