Organ dysfunction syndrome and mitochondrial adaptation in the septic patient

The ability to maintain an adequate energy balance and to respond and adapt to environmental stress at the cellular level are cornerstones for the survival and evolution of organisms. Therefore, in the presence of various factors, a cellular protection response is triggered by activation of mitochondrial function-dependent signaling. However, this essential reaction for individual cell survival can be detrimental to organ function (maladaptation), transforming the close balance between the two into the pathogenetic axis of organ dysfunction and eventual recovery in septic patients. Macrocirculatory and microcirculatory disruption undoubtedly contributes to organ dysfunction in the early stage of septic shock, while intrinsic metabolic-bioenergetic failure (cytopathic hypoxia) perpetuates inadequate cellular function. Therefore, mitochondrial dysfunction is a key process in the induction of multiple organ dysfunction syndrome in the septic patient. This syndrome can be considered as a complex hypometabolic adaptive phenomenon in the face of excessive and prolonged inflammatory stimulus to achieve regulation of energy homeostasis and preservation of organ function. In the future, there should be a transition from the current consensus therapeutic options, which are limited to control of the infectious focus, hemodynamic and life support, to metabolic resuscitation based on the molecular and genetic alterations triggered by the infection.