Mitochondrial complex II and reactive oxygen species in disease and therapy

Redox Rep. 2020 Dec;25(1):26-32. doi: 10.1080/13510002.2020.1752002.

Abstract

Increasing evidence points to the respiratory Complex II (CII) as a source and modulator of reactive oxygen species (ROS). Both functional loss of CII as well as its pharmacological inhibition can lead to ROS generation in cells, with a relevant impact on the development of pathophysiological conditions, i.e. cancer and neurodegenerative diseases. While the basic framework of CII involvement in ROS production has been defined, the fine details still await clarification. It is important to resolve these aspects to fully understand the role of CII in pathology and to explore its therapeutic potential in cancer and other diseases.

Keywords: OXPHOS; Respiratory complex II; cancer; mitochondria; reactive oxygen species; succinate; succinate dehydrogenase; tricarboxylic acid cycle.

Publication types

  • Review

MeSH terms

  • Animals
  • Electron Transport
  • Electron Transport Complex II / metabolism*
  • Humans
  • Mitochondria / metabolism
  • Mitochondria / pathology*
  • Mitochondrial Diseases / drug therapy
  • Mitochondrial Diseases / metabolism
  • Mitochondrial Diseases / pathology*
  • Molecular Targeted Therapy*
  • Reactive Oxygen Species / metabolism*

Substances

  • Reactive Oxygen Species
  • Electron Transport Complex II

Grants and funding

This work was supported by the Czech Science Foundation [grant numbers 19-20553S and 20-18513S], the institutional support of the Institute of Biotechnology RVO:86652036, and by the BIOCEV European Regional Development Fund CZ.1.05/1.1.00/02.0109.