The main role of mitochondria is to produce adenosine triphosphate (ATP) through the oxidative phosphorylation system for maintenance of normal cellular function. However, these organelles participate in several biochemical pathways other than ATP production, as for instance gluconeogenesis in liver and kidney, glyceroneogenesis in adipose tissue, and urea cycle in liver, to cite a few. Furthermore, mitochondria play a pivotal role in cell fate, since proapoptotic signals may be released from mitochondria in some circumstances. Also, it has been demonstrated that mitochondrial physiology may be altered due to extracellular signals, as for example, the level of neurotrophins, hormones, nutrients, and pharmacological toxicants in both macro- and microenvironments. Then, mitochondrial function changes as the necessities of the cells, but some molecules may induce mitochondrial dysfunction by interacting with the organelle and causing a decrease in ATP synthesis, an increase in reactive species production (e.g., free radicals), and/or the release of proapoptotic factors, for example.

We are particularly interested in manuscripts that report the results of investigations regarding the role of mitochondrial dysfunction in neurodegenerative diseases, proinflammatory processes (sepsis, trauma, infection, burn, and others), nutritional abnormalities, tumors, and disturbances affecting hepatic, renal, cardiovascular, immune, and gastrointestinal systems. Furthermore, manuscripts dealing with the role of bioactive molecules, pharmacological agents, and toxicants on mitochondrial function and dysfunction are welcome. Potential topics include, but are not limited to:

• Mitochondrial dysfunction and related signaling pathways
• Mitochondrial reactive species production (including free radicals) and antioxidant defenses
• Alterations in mitochondrial structure, metabolism, and/or physiology
• Interaction of mitochondria with other organelles
• Bioactive molecules and mitochondrial dysfunction
• Methods to access mitochondrial function
• Future strategies to treat mitochondrial dysfunction

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