Endogenous ligand for the apelin receptor (APLNR) (By similarity). Hormone required for mesendodermal differentiation, blood vessels formation and heart morphogenesis during early development and for adult cardiovascular homeostasis (PubMed:28371822, PubMed:28854362, PubMed:28890073, PubMed:28663440). Drives internalization of the APLNR (By similarity). Acts as a motogen by promoting mesendodermal cell migration during gastrulation by binding and activating APLNR (By similarity). Acts as an early embryonic regulator of cellular movement with a role in migration and development of cardiac progenitor cells (PubMed:28854362). May act as a chemoattractant for the activation of angioblast migration toward the embryonic midline, i.e. the position of the future vessel formation, during vasculogenesis (By similarity). Positively regulates sinus venosus (SV)-derived endothelial cells migration into the developing heart to promote coronary blood vessel sprouting (PubMed:28890073). Plays a role in placental vascular development; promotes placental trophoblast invasion and spiral artery remodeling in the uterus (PubMed:28663440). Involved in the regulation of maternal cardiovascular homeostasis to prevent gestational hypertension and for potent cardioprotective functions during heart failure (PubMed:28371822, PubMed:28663440). Mediates myocardial contractility in an ERK1/2-dependent manner (By similarity). Interacts with APLNR. Found in blood plasma (By similarity). Found in serum of pregnant mice, peaking at midgestation; indicating a maternal and zygotic origin of circulating APELA during pregnancy (PubMed:28663440). Expressed in the placenta (PubMed:28663440). Expressed in syncytiotrophoblasts of the placenta labyrinth at 10.5 dpc (PubMed:28663440). Expressed in placental chorionic trophoblasts (at protein level) (PubMed:28663440). Expressed in a small population of epiblast cells in the distal half of the embryo at 7 dpc (PubMed:20153842, PubMed:28854362). Expressed in newly formed definitive endoderm cells in the proximal half of the embryo, while it is not present in extra-embryonic endoderm at 7.5 dpc (PubMed:20153842, PubMed:28854362). This expression pattern then changes to the ventral aspect of the developing foregut pocket and the entire hindgut pocket at 8.5 dpc, before becoming restricted to the foregut overlying the heart and the posterior-most hindgut (PubMed:20153842). Not detected in endothelial precursor cells of the yolk sac at 8 dpc (PubMed:28663440). Expressed in extraembryonic tissues as well as in the chorion at 8.25 dpc (PubMed:28854362). Expressed in endometrial stroma of the uterus of pregnant mice at 8.5 dpc (PubMed:28663440). Expressed in the developing heart, caudal neural tube and trophobasts at 9 dpc (PubMed:28663440). Expressed in the chorionic plate of the chorioallantoic placenta at 9 dpc (PubMed:28663440). Expressed in the posterior half of the ventral neural tube at 9.25 dpc (PubMed:20153842). Expressed in trophoblast cells at the periphery of the placenta at 9.5 dpc (PubMed:28854362). Expressed in collecting ducts of the kidney of pregnant mice at 10.5 dpc (PubMed:28663440). Expressed in the epicardium of the developing heart at 11.5 dpc (PubMed:26611206, PubMed:28890073). Expressed weakly in the adult heart (PubMed:26611206). Expressed in endothelial cells and fibroblasts and weakly in cardiomyocytes (PubMed:26611206). Expressed during early embryonic development from the two cell to blastocyst stages (PubMed:28663440). Expressed in populations of the definitive endoderm from 7 to 8.5 dpc (PubMed:20153842). Up-regulated following myocardial infarction (MI) (at protein level) (PubMed:26611206). Mice lacking APELA are not represented at the expected Mendelian ratios (PubMed:28854362, PubMed:28663440). Mutant embryos exhibit around 10% to 50% incidence of incomplete penetrance of embryonic lethality (PubMed:28854362, PubMed:28663440). Fetal death is increased especially in mothers devoid of all Apela expression (PubMed:28663440). Mutant embryos show extraembryonic tissues anomalies, such as ectopic anterior chorion, mesoderm yolk sac and blood island protrusions and reduced allantois thickness at 8.25 dpc (PubMed:28854362). Mutant embryos show improper establishment of the fetal-maternal circulation, such as underdeveloped yolk sac vasculature, embryonic vascular malformations and impaired cardiac tube looping at 9.5 and 10.5 dpc (PubMed:28854362, PubMed:28663440). Show also defect in somitic vasculature at 10.5 dpc. The heart of mutant embryos show reduced coronary vessel growth at 13.5 dpc and 15.5 dpc (PubMed:28890073). The placenta of mutant pregnant mice show decreased labyrinth thickness, poor vasculature and decreased cell proliferation (PubMed:28663440). Mutant pregnant mice that survived to adulthood developed preeclampsia, including increased systolic blood pressure, proteinuria, and glomerular endotheliosis (PubMed:28663440). Mutant embryos show altered expression of several erythroid and myeloid progenitor genes at 7.5 dpc (PubMed:28854362). Mutant embryos show increased expression of hypoxia-related genes in the placenta at 10.5 (PubMed:28663440). Double knockout mice of APELA and APLN genes exhibit the same penetrance, embryonic lethality and cardiovascular malformations as single APELA knockout mice (PubMed:28854362). Belongs to the Elabela/Toddler family.