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.

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  • Additional Information
    • Source:
      Publisher: Elsevier Science Inc Country of Publication: United States NLM ID: 8008690 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-5169 (Electronic) Linking ISSN: 01969781 NLM ISO Abbreviation: Peptides Subsets: MEDLINE
    • Publication Information:
      Publication: New York, NY : Elsevier Science Inc.
      Original Publication: Fayetteville, N. Y., Ankho International.
    • Subject Terms:
      Apelin/*blood ; Bone Morphogenetic Proteins/*blood ; Fibrosis/*blood ; Growth Differentiation Factor 2/*blood ; Liver Cirrhosis/*blood; Adult ; Aged ; Female ; Fibrosis/pathology ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/pathology ; Male ; Middle Aged
    • Abstract:
      Background: The peptide apelin is expressed in human healthy livers and is implicated in the development of hepatic fibrosis and cirrhosis. Mutations in the bone morphogenetic protein receptor type II (BMPR-II) result in reduced plasma levels of apelin in patients with heritable pulmonary arterial hypertension. Ligands for BMPR-II include bone morphogenetic protein 9 (BMP9), highly expressed in liver, and BMP10, expressed in heart and to a lesser extent liver. However, it is not known whether reductions in BMP9 and/or BMP10, with associated reduction in BMPR-II signalling, correlate with altered levels of apelin in patients with liver fibrosis and cirrhosis.
      Methods: Plasma from patients with liver fibrosis (n = 14), cirrhosis (n = 56), and healthy controls (n = 25) was solid-phase extracted using a method optimised for recovery of apelin, which was measured by ELISA.
      Results: Plasma apelin was significantly reduced in liver fibrosis (8.3 ± 1.2 pg/ml) and cirrhosis (6.5 ± 0.6 pg/ml) patients compared with controls (15.4 ± 2.0 pg/ml). There was no obvious relationship between apelin and BMP 9 or BMP10 previously measured in these patients. Within the cirrhotic group, there was no significant correlation between apelin levels and disease severity scores, age, sex, or treatment with β-blockers.
      Conclusions: Apelin was significantly reduced in plasma of patients with both early (fibrosis) and late-stage (cirrhosis) liver disease. Fibrosis is more easily reversible and may represent a potential target for new therapeutic interventions. However, it remains unclear whether apelin signalling is detrimental in liver disease or is beneficial and therefore, whether an apelin antagonist or agonist have clinical use.
      (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)
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    • Grant Information:
      RG/19/3/34265 United Kingdom BHF_ British Heart Foundation; TG/18/4/33770 United Kingdom BHF_ British Heart Foundation; WT107715/Z/15/Z United Kingdom WT_ Wellcome Trust; SP/12/12/29836 United Kingdom BHF_ British Heart Foundation; RG/13/4/30107 United Kingdom BHF_ British Heart Foundation; MC_PC_14116 United Kingdom MRC_ Medical Research Council
    • Contributed Indexing:
      Keywords: Apelin; Apelin receptor; BMP10; BMP9; Fibrosis; Liver cirrhosis; Liver disease
    • Accession Number:
      0 (Apelin)
      0 (BMP10 protein, human)
      0 (Bone Morphogenetic Proteins)
      0 (GDF2 protein, human)
      0 (Growth Differentiation Factor 2)
    • Publication Date:
      Date Created: 20201110 Date Completed: 20211203 Latest Revision: 20240214
    • Publication Date:
      20240214
    • Accession Number:
      PMC7883214
    • Accession Number:
      10.1016/j.peptides.2020.170440
    • Accession Number:
      33171278