Mitochondrial superoxide dismutases-signals of distinction

Sumitra Miriyala, Aaron K. Holley, Daret K. St Clair

Research output: Contribution to journalArticlepeer-review

54 Scopus citations

Abstract

Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O2.-), the first member in a plethora of mitochondrial reactive oxygen species (ROS). Over the past decades, research has extended the prevailing view of mitochondrion well beyond the generation of cellular energy to include its importance in cell survival and cell death. In the normal state of a cell, endogenous antioxidant enzyme systems maintain the level of reactive oxygen species generated by the mitochondrial respiratory chain. Mammalian mitochondria are important to the production of reactive oxygen species, which underlie oxidative damage in many pathological conditions and contribute to retrograde redox signaling from the organelle to the cytosol and nucleus. Mitochondria are further implicated in various metabolic and aging-related diseases that are now postulated to be caused by misregulation of physiological systems rather than pure accumulation of oxidative damage. Thus, the signaling mechanisms within mitochondria, and between the organelle and its environment, have gained interest as potential drug targets. Here, we discuss redox events in mitochondria that lead to retrograde signaling, the role of redox events in disease, and their potential to serve as therapeutic targets.

Original languageEnglish
Pages (from-to)181-190
Number of pages10
JournalAnti-Cancer Agents in Medicinal Chemistry
Volume11
Issue number2
DOIs
StatePublished - Feb 2011

Keywords

  • Apoptotic pathways
  • MnSOD
  • Oxidative modification
  • Oxidative stress
  • Redox signaling
  • Retrograde signaling
  • TOR signaling
  • mtDNA

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology
  • Cancer Research

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