Potential Clinical Targets in Hepatopulmonary Syndrome: Lessons From Experimental Models

Sarah Raevens, Michael B. Fallon

Research output: Contribution to journalReview article

5 Scopus citations

Abstract

Hepatopulmonary syndrome (HPS) is a relatively common and potentially severe pulmonary complication of cirrhosis with increased risk of mortality. In experimental models, a complex interaction between pulmonary endothelial cells, monocytes, and the respiratory epithelium, which produces chemokines, cytokines, and angiogenic growth factors, causes alterations in the alveolar microvasculature, resulting in impaired oxygenation. Model systems are critical for evaluating mechanisms and for preclinical testing in HPS, due to the challenges of evaluating the lung in the setting of advanced liver disease in humans. This review provides an overview of current knowledge and recent findings in the rodent common bile duct ligation model of HPS, which recapitulates many features of human disease. We focus on the concepts of endothelial derangement, monocyte infiltration, angiogenesis, and alveolar type II cell dysfunction as main contributors and potential targets for therapy.

Original languageEnglish (US)
Pages (from-to)2016-2028
Number of pages13
JournalHepatology
Volume68
Issue number5
DOIs
StatePublished - Nov 2018
Externally publishedYes

ASJC Scopus subject areas

  • Hepatology

Fingerprint Dive into the research topics of 'Potential Clinical Targets in Hepatopulmonary Syndrome: Lessons From Experimental Models'. Together they form a unique fingerprint.

  • Cite this