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Palabras clave – provistas por la editorial

pregnancy-induced CVD; chronic venous disease; proinflammatory cytokines; hypertensive vascular disorder; MeSH; preeclampsia; MenSCs; trophoblast invasion; galectin; maternal–fetal interface; pathologic pregnancy; gestational diabetes mellitus; fetal growth restriction; preterm birth; FGF2; angiogenesis; oxidative stress; L-NAME; gene expression; placenta; cardiovascular microRNAs; early pregnancy; prediction; screening; whole peripheral venous blood; chorionic villus sampling; congenital malformations; prenatal testing transcriptome sequencing; endometriosis; pyroptosis; PGE2; cell migration; glucose uptake; SLC2A3; SLC2A1; insulin; glucagon; infertility; assisted reproductive technology; implantation failure; endometrium immunomodulation; blood–brain barrier; endothelium; fetal hypoxia; neuronal damage; tight junctions; tight junction proteins; IL-6; IL-8; inflammation; pregnancy; pregnancy complications; microRNAs; miRNAs; small RNA sequencing; small RNA-seq; sPTD; miR-23b-5p; miR-125a-5p; miR-4732-5p; primary hyperparathyroidism; forensic; pulmonary metastatic calcification; B cells; idiopathic recurrent pregnancy loss; reproductive immunology; meta-analysis; ficolin-2; FCN2; newborn; neonate; prematurity; single nucleotide polymorphism; very low birthweight; diabetes mellitus; human; RNA sequencing; CD24; placental-derived immortalized cells; JEG-3 cells; BeWo cells; STOX1-A/B; in vitro preeclampsia models; immune tolerance; amino acid transporters; SLC38A1; SLC38A2; SLC38A4; ischemic placental syndrome; soluble endoglin (sEng); soluble fms-like tyrosine kinase-1 (sFlt-1); placental growth factor (PlGF); sFlt-1/PlGF and sFlt-1*sEng/PlGF ratios; pregnancy adverse outcomes; n/a