RAGE regulates autophagy and apoptosis following oxidative injury

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

Research output: Contribution to journalShort survey

54 Scopus citations

Abstract

The receptor for advanced glycation end products (RAGE) plays a crucial role in several disease processes including diabetes, inflammation and cancer. Compared with apoptosis ("programmed cell death"), autophagy is a genetically programmed, evolutionarily conserved cell survival process that degrades long-lived cellular proteins and organelles ("programmed cell survival"). Recently we reported that RAGE is an important regulator of oxidative stress in pancreatic cancer cells. Upregulation of RAGE expression by the nuclear factor (NF)κB pathway decreases reactive oxygen species (ROS)-induced oxidative injury. In contrast, suppression of RAGE expression increases pancreatic tumor cell sensitivity to oxidative injury. Furthermore, RAGE is a positive regulator of autophagy and a negative regulator of apoptosis during oxidative stress. These findings provide insight into how crosstalk between apoptosis and autophagy is mediated via ROS signaling with a process involving RAGE.

Original languageEnglish (US)
Pages (from-to)442-444
Number of pages3
JournalAutophagy
Volume7
Issue number4
DOIs
StatePublished - Apr 2011
Externally publishedYes

Keywords

  • Apoptosis
  • Autophagy
  • Drug resistance
  • NFκB
  • Oxidative stress
  • RAGE

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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