Mitochondria are involved in a great number of important physiological and pathophysiological processes. Increasing evidence supports a role for mitochondrial dysfunction in many human diseases including inherited diseases as well as environment-linked diseases such as cardiac diseases, neuropathies, cancer, and obesity. Mitochondrial dysfunction manifests by energetic failure, oxidative stress, lipid metabolism abnormalities, and apoptosis sensitization. Therefore, the basic understanding of cytoprotective mechanisms at the mitochondrial level constitutes an important challenge. Plausible implication should be to better diagnose, classify the risks, and treat diseases involving a mitochondrial dysfunction. Promising therapeutic strategies include but are not limited to metabolic therapy or apoptosis inhibition.

We invite authors to submit original research and review articles that seek to improve the understanding of mitochondrial function in cytoprotection. We are especially interested in articles that explore the possibility of exploiting this knowledge of mitochondrial function for future translational purposes, that is, diagnosis or treatment. Potential topics include, but are not limited to:

• Mitochondrial function (energy, apoptosis, fission/fusion, OXPHOS, ROS, and lipid metabolism)
• Mitochondria in pathology (AIDS, cardiovascular diseases, diabetes, neonatal brain damage, neurodegeneration, stroke, etc.)
• Environmental stress (pro-oxidant stress, intoxication, and pollutants)
• Integrated methodological approaches (system biology and integrative physiology)
• Pharmacological approaches to target mitochondria

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