Natriuretic peptide metabolism, clearance and degradation

Research output: Contribution to journalReview article

169 Citations (Scopus)

Abstract

Atrial natriuretic peptide, B-type natriuretic peptide and C-type natriuretic peptide constitute a family of three structurally related, but genetically distinct, signaling molecules that regulate the cardiovascular, skeletal, nervous, reproductive and other systems by activating transmembrane guanylyl cyclases and elevating intracellular cGMP concentrations. This review broadly discusses the general characteristics of natriuretic peptides and their cognate signaling receptors, and then specifically discusses the tissue-specific metabolism of natriuretic peptides and their degradation by neprilysin, insulin-degrading enzyme, and natriuretic peptide receptor-C. Natriuretic peptides are a family of three related pleiotropic signaling factors that bind and activate transmembrane guanylyl cyclases. This review initially discusses the general characteristics of natriuretic peptides and their receptors. The tissue specific metabolism of natriuretic peptides and their degradation by individual proteases and natriuretic peptide receptor C-mediated internalization are then more specifically discussed.

Original languageEnglish (US)
Pages (from-to)1808-1817
Number of pages10
JournalFEBS Journal
Volume278
Issue number11
DOIs
StatePublished - Jun 1 2011

Fingerprint

Natriuretic Peptides
Metabolism
Degradation
Guanylate Cyclase
Insulysin
C-Type Natriuretic Peptide
Tissue
Neprilysin
Peptide Receptors
Brain Natriuretic Peptide
Atrial Natriuretic Factor
Peptide Hydrolases
Molecules
atrial natriuretic factor receptor C

Keywords

  • ANF
  • B-type natriuretic peptide (BNP)
  • atrial natriuretic peptide (ANP)
  • cGMP
  • cardiovascular disease
  • endochondrial ossification
  • neprilysin
  • proteolysis
  • receptor internalization

Cite this

Natriuretic peptide metabolism, clearance and degradation. / Potter, Lincoln R.

In: FEBS Journal, Vol. 278, No. 11, 01.06.2011, p. 1808-1817.

Research output: Contribution to journalReview article

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