III. Intracellular signaling in response to toxic liver injury

B. E. Jones, M. J. Czaja

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Toxin-induced liver injury was formerly considered a passive biochemical event, but recent evidence has demonstrated that signal transduction pathways actively modulate the hepatocyte's response to this form of injury. Investigations have examined the effects of a variety of toxins on the activation of receptor-coupled signal transduction, mitogen-activated protein kinases, and Fas signaling, as well as the generation of second messengers such as ceramide and nitric oxide. Many of these pathways culminate in the activation of transcription factors such as activator protein-1, c-Myc, or nuclear factor-κB. This Themes article discusses the effects of toxic injury on these signaling pathways and their known functions in regulating hepatocyte death and proliferation following injury.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume275
Issue number5 38-5
StatePublished - 1998

Fingerprint

Poisons
Liver
Wounds and Injuries
Hepatocytes
Signal Transduction
Ceramides
Transcription Factor AP-1
Second Messenger Systems
Mitogen-Activated Protein Kinases
Nitric Oxide
Transcription Factors

Keywords

  • Activator protein-1
  • C-Myc
  • Ceramide
  • Fas
  • Mitogen-activated protein kinasse
  • Nitric oxide
  • Nuclear factor-κB

ASJC Scopus subject areas

  • Gastroenterology
  • Physiology

Cite this

III. Intracellular signaling in response to toxic liver injury. / Jones, B. E.; Czaja, M. J.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 275, No. 5 38-5, 1998.

Research output: Contribution to journalArticle

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