CONICET | Buscador de Institutos y Recursos Humanos

Septic patients with myocardial dysfunction have a 3-fold increase in mortality compared with patients without cardiovascularimpairment, and usually show myocarditis, disruption of the contractile apparatus, increased amounts of interstitialcollagen, and damaged mitochondria. The presence of nitric oxide and cytokines in cardiac tissue constitute the molecularmarkers and the intracellular messengers of inflammatory conditions in the heart due to the onset of sepsis and endotoxemia,derived from the nuclear factor-κB pathway activation and proinflammatory gene transcription. Sepsis occurs withan exacerbated inflammatory response that damages tissue mitochondria and impaired bioenergetic processes. The heartconsumes 20?30 times its own weight in adenosine triphosphate every day, and 90% of this molecule is derived frommitochondrial oxidative phosphorylation. Cardiac energy management is comprised in sepsis and endotoxemia; both adeficit in energy production and alterations in the source of energy substrates are believed to be involved in impaired cardiacfunction. Although several hypotheses try to explain the molecular mechanisms underlying the complex conditionof sepsis and endotoxemia, the current view is that these syndromes are the result of an intricate balance between prevailinglevels of mitochondrial stress, biogenesis/autophagy signaling and mitochondria quality control processes, rather on asingle factor. The aim of this review is to discuss current hypothesis of cardiac dysfunction related to energy metabolismand mitochondrial function in experimental models of sepsis and endotoxemia, and to introduce the importance of lipids(mainly cardiolipin) in the mechanism of cardiac energy mismanagement in these inflammatory conditions