Repeated Measurement of the Novel Atrial Biomarker BMP10 (Bone Morphogenetic Protein 10) Refines Risk Stratification in Anticoagulated Patients With Atrial Fibrillation: Insights From the ARISTOTLE Trial.
Homozygous GDF2 nonsense mutations result in a loss of circulating BMP9 and BMP10 and are associated with either PAH or an ""HHT-like"" syndrome in children.
Plasma levels of apelin are reduced in patients with liver fibrosis and cirrhosis but are not correlated with circulating levels of bone morphogenetic protein 9 and 10.
Reduced circulating BMP10 and BMP9 and elevated endoglin are associated with disease severity decompensation and pulmonary vascular syndromes in patients with cirrhosis.
BMP10 was able to promote cardiomyocyte survival and prevent cardiac adverse remodeling. Additional experiments with the de novo activation of BMP10 in the postnatal heart and the treatment of recombinant human BMP10 (rhBMP10) further confirmed this observation. A novel activity of BMP10 is in activating both SMAD- and STAT3- mediated signaling pathways.
Findings demonstrate that GDF2 mutations result in BMP9 loss of function and are likely causal for pulmonary arterial hypertension. These mutations lead to reduced circulating levels of both BMP9 and BMP10.
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