CONICET | Buscador de Institutos y Recursos Humanos

Abstract: Sepsis is the manifestation of the immune and inflammatory response toinfection that may ultimately result in multi organ failure. Despite the therapeutic strategiesthat have been used up to now, sepsis and septic shock remain a leading cause of death incritically ill patients. Myocardial dysfunction is a well-described complication of severesepsis, also referred to as septic cardiomyopathy, which may progress to right and leftventricular pump failure. Many substances and mechanisms seem to be involved inmyocardial dysfunction in sepsis, including toxins, cytokines, nitric oxide, complementactivation, apoptosis and energy metabolic derangements. Nevertheless, the preciseunderlying molecular mechanisms as well as their significance in the pathogenesis ofseptic cardiomyopathy remain incompletely understood. A well-investigated abnormalityin septic cardiomyopathy is mitochondrial dysfunction, which likely contributes to cardiacdysfunction by causing myocardial energy depletion. A number of mechanisms have beenproposed to cause mitochondrial dysfunction in septic cardiomyopathy, although it remainscontroversially discussed whether some mechanisms impair mitochondrial function or serveto restore mitochondrial function. The purpose of this review is to discuss mitochondrialmechanisms that may causally contribute to mitochondrial dysfunction and/or may representadaptive responses to mitochondrial dysfunction in septic cardiomyopathy.