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Mitochondria as a Central Hub in the Cellular Response to Redox-Active Environmental Pollutants

Call for Papers

Mitochondria control critical cellular functions, including redox homeostasis, apoptosis, and autophagy. Several pathologies arise from the dysregulated production of reactive oxygen species (ROS) within mitochondria due to internal or external stimuli. ROS-derived oxidative stress is acknowledged as one of the major mechanisms underlying pollutant-induced toxicity. In particular, a number of environmental agents can target mitochondria by directly or indirectly promoting the generation of ROS and other redox-dependent signaling molecules. However, ROS are also known to mediate transduction mechanisms that allow survival in changed environmental conditions, thus resulting in adaptive responses.

The increasing presence of chemical and physical pollutants in today’s domestic, occupational, and outdoor environments highlights the need for an extensive research effort aimed at identifying the molecular players involved in the critical decisions that direct cells exposed to environment-derived pollution towards dysfunction, failure, or survival. In this context, particular attention should be paid to how pollution might impact the behavior of cells which are highly dependent on oxidative processes (e.g., neurons) or whose control of redox homeostasis is impaired (e.g., tumor cells). This would shed novel light on the positive association between increased environmental pollution and the growth of chronic diseases of great public concern (e.g., neurodegeneration and cancer).

Based on these data, we invite researchers to contribute to this topic with original studies and review articles focused on mitochondrion-directed response to redox-active environmental pollutants, as well as on novel imaging techniques for noninvasive assessment of mitochondrial function in live cells. Articles describing new approaches to limit or prevent mitochondrial dysregulation after exposure to environment-derived pollutants are also welcome. In addition, researches of new strategies to interfere with the molecular checkpoints involved in the crossroad between mitochondrial malfunction and adaptive response, especially in neuron-derived or cancer cells, are highly appreciated.

Potential topics include but are not limited to the following:

  • In vitro and in vivo studies on the effects of particulate matter (PM), inorganic components, trace and heavy metals, organic solvents, atmospheric gases, and electromagnetic radiation on the major markers of mitochondrial function and/or redox status, as well as on mitochondria-controlled autophagic processes
  • Use of synthetic or natural compounds to limit or prevent mitochondrial dysfunction induced by redox-active environment-derived pollution
  • Studies using in vivo imaging techniques to analyze the dynamics, metabolism, energy state, redox-dependent signaling, and oxidative damage on mitochondria of animals or humans exposed to environment-derived chemicals and physical pollutants
  • Alteration of mitochondrial and cellular functions in high-energy-demanding cells upon treatment with environmental pollutants
  • Alteration of responsiveness to prooxidant treatments in tumor/cancer cells following exposure to environment-derived pollutants, with possible involvement of changes in mitochondrial metabolism and/or dynamics, including but not limited to fission and fusion

Authors can submit their manuscripts through the Manuscript Tracking System at

Submission DeadlineFriday, 29 June 2018
Publication DateNovember 2018

Papers are published upon acceptance, regardless of the Special Issue publication date.

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