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Ecto-5'-nucleotidase (CD73)-mediated extracellular adenosine production plays a critical role in hepatic fibrosis

Zhongsheng Peng1, Patricia Fernandez, Tuere Wilder

  • 1Department of Medicine, Division of Clinical Pharmacology, New York University School of Medicine, New York, New York 10016, USA.

Nucleosides, Nucleotides & Nucleic Acids
|July 5, 2008
PubMed

Insights

Adenosine plays a key role in liver fibrosis. Toxin-induced liver fibrosis relies on the extracellular conversion of adenine nucleotides to adenosine, mediated by ecto-5

Area of Science:

  • Biochemistry
  • Hepatology
  • Pharmacology

Background:

  • Adenosine and its receptors are implicated in hepatic fibrosis.
  • Previous research suggests a role for adenosine in liver disease progression.

Purpose of the Study:

  • To review evidence linking toxin-induced hepatic adenosine increases to hepatic fibrosis.
  • To elucidate the mechanism of adenosine generation in toxin-induced liver fibrosis.

Main Methods:

  • Review of existing scientific literature.
  • Analysis of biochemical pathways involved in adenosine metabolism.
  • Examination of studies on toxin-induced liver injury.

Main Results:

  • Toxin exposure increases hepatic adenosine concentrations.
  • Adenosine is generated from adenine nucleotides via ecto-5'nucleotidase.
  • Extracellular conversion of adenine nucleotides to adenosine is crucial for adenosine-mediated, toxin-induced hepatic fibrosis.

Conclusions:

  • Hepatic adenosine generation from extracellular adenine nucleotides is a key mechanism in toxin-induced liver fibrosis.
  • Targeting ecto-5'nucleotidase or extracellular adenosine may offer therapeutic strategies for liver fibrosis.

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