Autophagy in nonalcoholic steatohepatitis

Muhammad Amir, Mark J. Czaja

Research output: Contribution to journalReview articlepeer-review

131 Scopus citations

Abstract

Autophagy is a critical pathway for the degradation of intracellular components by lysosomes. Established functions for both macroautophagy and chaperone-mediated autophagy in hepatic lipid metabolism, insulin sensitivity and cellular injury suggest a number of potential mechanistic roles for autophagy in nonalcoholic steatohepatitis (NASH). Decreased autophagic function in particular may promote the initial development of hepatic steatosis and progression of steatosis to liver injury. Additional functions of autophagy in immune responses and carcinogenesis may also contribute to the development of NASH and its complications. The impairment in autophagy that occurs with cellular lipid accumulation, obesity and aging may therefore have an important impact on this disease, and agents to augment hepatic autophagy have therapeutic potential in NASH.

Original languageEnglish (US)
Pages (from-to)159-166
Number of pages8
JournalExpert Review of Gastroenterology and Hepatology
Volume5
Issue number2
DOIs
StatePublished - Apr 1 2011

Keywords

  • chaperone-mediated autophagy
  • insulin sensitivity
  • liver injury
  • macroautophagy
  • nonalcoholic fatty liver disease
  • oxidative stress

ASJC Scopus subject areas

  • Hepatology
  • Gastroenterology

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