Molecular therapy for hepatic injury and fibrosis: Where are we?

Colette C. Prosser, Roy D. Yen, Jian Wu

Research output: Contribution to journalArticle

83 Scopus citations

Abstract

Hepatic fibrosis is a wound healing response, involving pathways of inflammation and fibrogenesis. In response to various insults, such as alcohol, ischemia, viral agents, and medications or hepatotoxins, hepatocyte damage will cause the release of cytokines and other soluble factors by Kupffer cells and other cell types in the liver. These factors lead to activation of hepatic stellate cells, which synthesize large amounts of extracellular matrix components. With chronic injury and fibrosis, liver architecture and metabolism are disrupted, eventually manifesting as cirrhosis and its complications. In addition to eliminating etiology, such as antiviral therapy and pharmacological intervention, it is encouraging that novel strategies are being developed to directly address hepatic injury and fibrosis at the subcellular and molecular levels. With improvement in understanding these mechanisms and pathways, key steps in injury, signaling, activation, and gene expression are being targeted by molecular modalities and other molecular or gene therapy approaches. This article intends to provide an update in terms of the current status of molecular therapy for hepatic injury and fibrosis and how far we are from clinical utilization of these new therapeutic modalities.

Original languageEnglish (US)
Pages (from-to)509-515
Number of pages7
JournalWorld Journal of Gastroenterology
Volume12
Issue number4
StatePublished - Jan 28 2006

Keywords

  • Fibrosis
  • Gene therapy
  • Hepatic stellate cell
  • Hepatocyte
  • Injury

ASJC Scopus subject areas

  • Gastroenterology

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