Apelin receptor early endogenous ligand
experimentalAlso known as: Protein Elabela, Protein Toddler, APELA, P0DMC3
Apelin receptor early endogenous ligand (APELA), also known as Elabela or Toddler, is a peptide hormone that acts as an endogenous ligand for the G protein-coupled apelin receptor (APJ). Its mechanism involves binding to APJ to activate downstream signaling pathways, including Gαi/o and β-arrestin recruitment, which modulate cardiovascular function and fluid homeostasis. APELA is particularly critical during embryonic development, where it regulates cell migration and heart formation, and in adulthood, it contributes to vascular tone regulation and blood pressure control. Key research findings indicate that APELA is expressed in the heart, kidney, and vasculature, and its signaling is essential for early cardiac morphogenesis. Studies have shown that APELA deficiency leads to impaired cardiovascular development and fluid balance disturbances. Experimental models suggest that APELA may have therapeutic potential in conditions such as hypertension, heart failure, and preeclampsia, though its precise physiological roles are still being elucidated. Clinical relevance remains exploratory, with ongoing investigations into APELA as a biomarker or therapeutic target for cardiovascular and renal diseases. Its role in fluid homeostasis suggests potential applications in managing edema or electrolyte imbalances. For research purposes only — not medical advice.
Key data
MRFQQFLFAFFIFIMSLLLISGQRPVNLTMRRKLRKHNCLQRRCMPLHSRVPFPMechanism of action
Peptide hormone that functions as endogenous ligand for the G protein-coupled apelin receptor (APLNR/APJ), that plays a role in the regulation of normal cardiovascular function and fluid homeostasis (PubMed:25639753, PubMed:28137936, PubMed:35817871). Functions as a balanced agonist activating both G(i) protein pathway and beta-arrestin pathway of APLNR (PubMed:35817871). Downstream G proteins activation, apelin can inhibit cAMP production and activate key intracellular effectors such as ERKs (PubMed:35817871). On the other hand, APLNR activation induces beta-arrestin recruitment to the membrane leading to desensitization and internalization of the receptor (PubMed:35817871). Required for mesendodermal differentiation, blood vessels formation and heart morphogenesis during early development and for adult cardiovascular homeostasis (PubMed:25639753, PubMed:28137936). Acts as a motogen by promoting mesendodermal cell migration during gastrulation by binding and activating APLNR. Acts as an early embryonic regulator of cellular movement with a role in migration and development of cardiac progenitor cells. 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. Positively regulates sinus venosus (SV)-derived endothelial cells migration into the developing heart to promote coronary blood vessel sprouting. Plays a role in placental vascular development; promotes placental trophoblast invasion and spiral artery remodeling in the uterus. Involved in the regulation of maternal cardiovascular homeostasis to prevent gestational hypertension and for potent cardioprotective functions during heart failure. Mediates myocardial contractility in an ERK1/2-dependent manner (By similarity)
Research & studies
LIN28B is expressed 1300-fold higher than LIN28A in human term placenta and is the predominant paralog in trophoblast cultures.; LIN28B mRNA and protein levels are significantly reduced in preeclamptic placentas compared to normal placentas.; LIN28B overexpression increases trophoblast cell proliferation, migration, and invasion, while knockdown reduces proliferation and suppresses syncytin 1 and ELABELA expression.; Hypoxia decreases LIN28B expression and increases TNF-α, linking reduced LIN28B to impaired trophoblast function and inflammation in preeclampsia.
ELABELA mRNA was unchanged in 82 preeclamptic placentas compared with 82 matched controls (mean difference, 0.53%; P = 0.78).; Circulating ELABELA concentrations did not differ between 32 women with preterm preeclampsia and 32 matched controls (median difference, 8.0 pg/mL; P = 0.43).; Soluble FLT1 mRNA and circulating levels were significantly increased in preeclampsia, confirming the known association.; The findings contradict the hypothesized clinical relevance of ELABELA from murine preeclampsia models.
Frequently asked questions
What is Apelin receptor early endogenous ligand?
Apelin receptor early endogenous ligand (APELA), also known as Elabela or Toddler, is a peptide hormone that acts as an endogenous ligand for the G protein-coupled apelin receptor (APJ). Its mechanism involves binding to APJ to activate downstream signaling pathways, including Gαi/o and β-arrestin recruitment, which mo
How does Apelin receptor early endogenous ligand work?
Peptide hormone that functions as endogenous ligand for the G protein-coupled apelin receptor (APLNR/APJ), that plays a role in the regulation of normal cardiovascular function and fluid homeostasis (PubMed:25639753, PubMed:28137936, PubMed:35817871). Functions as a balanced agonist activating both G(i) protein pathway and beta-arrestin pathway of APLNR (PubMed:35817871). Downstream G proteins act
What is the research status of Apelin receptor early endogenous ligand?
Apelin receptor early endogenous ligand is currently classified as experimental, with 2 research references on record. This is for research purposes only and is not medical advice.
What is the molecular weight of Apelin receptor early endogenous ligand?
Apelin receptor early endogenous ligand has a molecular weight of approximately 6622 g/mol.
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