Metabolic regulation by HMGB1-mediated autophagy and mitophagy

Rui Kang, Kristen M. Livesey, Herbert J. Zeh, Michael T. Lotze, Daolin Tang

Research output: Contribution to journalArticle

51 Scopus citations

Abstract

Autophagy is a dynamic process for degradation of cytosolic components such as dysfunctional organelles and proteins and a means for generating metabolic substrates during periods of starvation. Mitochondrial autophagy ("mitophagy") is a selective form of autophagy, which is important in maintaining mitochondrial homeostasis. High mobility group box 1 (HMGB1) plays important intranuclear, cytosolic and extracellular roles in the regulation of autophagy. Cytoplasmic HMGB1 is a novel Beclin 1-binding protein active in autophagy. Extracellular HMGB1 induces autophagy, and this role is dependent on its redox state and receptor (Receptor for Advanced Glycation End products, RAGE) expression. Nuclear HMGB1 modulates the expression of heat shock protein β-1 (HSPB1/HSP27). As a cytoskeleton regulator, HSPB1 is critical for dynamic intracellular trafficking during autophagy and mitophagy. Loss of either HMGB1 or HSPB1 results in a phenotypically similar deficiency in mitophagy typified by mitochondrial fragmentation with decreased aerobic respiration and adenosine triphosphate (ATP) production. These findings reveal a novel pathway coupling autophagy and cellular energy metabolism.

Original languageEnglish (US)
Pages (from-to)1256-1258
Number of pages3
JournalAutophagy
Volume7
Issue number10
DOIs
StatePublished - Oct 2011
Externally publishedYes

Keywords

  • HMGB1
  • Metabolism
  • Mitochondria
  • Mitophagy
  • Small heat shock protein

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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