Mitochondrial Medicine

Abstract

Socrates: … And he who is most skilled in preventing or escaping from a disease is best able to create one? Polemarchus: True Socrates: And is he the best guard of a camp who is best able to steal a march upon the enemy? Polemarchus: Certainly Socrates: Then he who is a good keeper of everything is also a good thief? Polemarchus: That I suppose is to be inferred — —Plato, The Republic Reading Plato one might not be surprised by the apparent paradox in the ability of mitochondria to promote both life and death: On the one hand, they are the major producers of energy in the cell, and on the other hand, they can steal the life of their host “at will.” Mitochondria can sense the supply of fuel (they are important O2 sensors) and via the production of mediators (reactive O2 species [ROS]), communicate with critical effectors in the cell (like redox-sensitive ion channels in the membrane or the nucleus).1 In response to the needs of the cell, mitochondria produce both energy (ie, ATP) and heat, allowing the organism to work and keep a stable core temperature, facilitating optimal adaptation of eukaryotic cells to their environment. If the mitochondria cannot provide optimal adaptation to the metabolic needs and the environment, they have the ability to induce cell death (apoptosis). As strategic regulators of life and death, mitochondria are deeply involved in human disease, but the depth and breadth of mitochondria-based diseases is only now starting to be recognized.2 Article p 2492 Metabolism and apoptosis converge in mitochondria and are both recognized as playing a major role in disease. Primary metabolic abnormalities are now recognized in pulmonary and systemic vascular disease, and the apoptosis resistance seen in proliferative vascular remodeling might have a mitochondrial …