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The Role of Mitochondria in Oxidative Stress-Induced Cell Death

Call for Papers

Mitochondria are important players both in cell survival and cell death. In normal circumstances, they provide metabolic intermediates and energy in the form of ATP, but under stress conditions they initiate cell death programmes by releasing death-promoting factors into the cytoplasm. This second role of mitochondria is crucial for the cytotoxic activity of many anticancer agents. One of the important scenarios leading to cell death is a sudden increase of reactive oxygen species (ROS), which, acting either as signalling molecules or oxidants, may induce mitochondria to initiate apoptosis or commit the cell to a different form of regulated cell death known as necroptosis. In addition, owing to high electron fluxes within the electron transport chain, mitochondria themselves are the major cellular sites of ROS production, and mitochondrial status may, therefore, determine not only the magnitude of response to ROS but also the amount of ROS that is produced in the first place. In this way, mitochondria control two important aspects of oxidative stress-induced cell death, and understanding of mechanisms that govern ROS production and cell-death induction by ROS is the key to the development of new anticancer agents with selective toxicity to cancer cells. In addition, this understanding could also stimulate the introduction of new strategies to ameliorate negative effects of persistent ROS associated with mitochondrial dysfunction.

We invite authors to submit original research and review articles mapping the role of mitochondria in oxidative stress-induced cell death. We are interested in papers that describe factors defining the propensity of mitochondria to produce ROS in a basal state and in response to stimuli, as well as factors that determine apoptotic or necroptotic response to mitochondrially produced ROS. Potential topics include, but are not limited to:

  • The role of mitochondrial electron transport chain in ROS generation and cell death induction
  • The role of ROS detoxification in sensitivity to cell death
  • Signalling pathways modulated by mitochondrial ROS production
  • Signalling pathways that modulate mitochondrial ROS production
  • Mitochondria-targeted pro- and antioxidants
  • Therapeutic strategies modulating mitochondrial redox state

Before submission authors should carefully read over the journal’s Author Guidelines, which are located at http://www.hindawi.com/journals/omcl/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/omcl/mitox/ according to the following timetable:

Manuscript DueFriday, 24 January 2014
First Round of ReviewsFriday, 18 April 2014
Publication DateFriday, 13 June 2014

Lead Guest Editor

  • Jakub Rohlena, Institute of Biotechnology AS CR, Prague, Czech Republic

Guest Editors

  • Tomas Mracek, Institute of Physiology AS CR, Prague, Czech Republic
  • Erik Norberg, Karolinska Institute, stockholm, Sweden
  • Lubomir Prochazka, Veterinary Research Institute, Brno, Czech Republic
  • Marco Tomasetti, Department of Clinical and Molecular Sciences, Polytechnic University of Marche, Ancona, Italy