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  • Such analysis of mitochondrial function expected to be very


    Such analysis of mitochondrial function expected to be very important in septic patients. Mervyn Singer and his group review the current knowledge [] on the role of mitochondria in sepsis. Mitochondrial dysfunction has been suggested as a discriminator between survival and death. Importantly, an early analysis in sepsis is indispensable as sepsis rapidly worsens and treatment has to be immediate. Mitochondrial dysfunction has been suggested to contribute to sepsis induced cardiomyopathy as metabolic derangements are central in this disease. The authors describe the pathophysiology underlying myocardial dysfunction in sepsis and focus in their manuscript on mitochondrial processes. The analysis of metabolism and mitochondrial function and preservation of mitochondrial integrity and quality may be a basis for improved treatment in the future. The second manuscript of Sina Coldewey and her group [] addresses AMPK signaling in sepsis. This contribution is of interest because sphingosine-1-phosphate signaling in some endothelial Cycloheximide is mediated by the well-known metabolic sensor AMPK and thereby mediates stabilization of the endothelial barrier. In sepsis, breakdown of endothelial barrier is critical for organ failure and endothelial stabilization may thus prevent death. Whether sphingosine-1-phosphate signaling on AMPK affects substrate metabolism simultaneously remains an interesting question in this situation, but may have a high potential to explain metabolic changes in sepsis. Naturally, mitochondria as the hotspot for ATP generation and substrate use attract further attention in metabolic research. Thus, the article of Yan Burelle and his group [] presents an overview on mitochondrial quality control pathways. The authors indicate that mitochondrial quality control relies on multiple overlapping mechanisms. Mitochondrial proteases and chaperones process newly imported proteins but degrade non-assembled proteins as well. Protease involvement in mitochondrial unfolded protein response is discussed. Similarly, the ubiquitine-proteasome pathway and mitochondrial dynamics are presented as important quality control mechanisms in mitochondria. Mitochondria derived vesicles as new pathway for quality control is discussed and last but not least mitophagy is presented as well. Mitophagy pathways are reviewed in detail by ├ůsa Gustafsson and her group []. Canonical as well as non-canonical pathways of mitophagy are discussed and the link of these pathways to cardiac health is explored []. This important process selectively removes dysfunctional mitochondria as they may produce high amounts of reactive oxygen species (ROS) or induce apoptosis. The authors discuss Cycloheximide mitochondrial membrane dysfunction as an important component in initiating mitophagic processes. Mitochondrial membranes present with unique properties due to cardiolipin as a major component. The review of Peter Rehling and his group [] focuses on the role of cardiolipin in cardiac health and disease. The role of cardiolipin in mitochondrial biogenesis as well as morphology is addressed. Cardiolipin as the major membrane component also affects the function of the membrane associated respiratory chain. Furthermore, with its close proximity to places of ROS production, cardiolipin is easily oxidized in case ROS production becomes dysregulated, leading to changes in membrane morphology as well as respiratory chain function. Oxidative stress not only affects cardiolipin, but is regarded as a main contributor to damage in ischemia and reperfusion as well as in hypoxia. Ischemia/reperfusion is mainly seen in myocardial infarction but is also voluntarily induced in cardiac surgery procedures. A protection of the myocardium against such damages is highly needed as myocardial infarction is a main cause of death in western societies. Petra Kleinbongard and her group address in their review the question whether or not ischemic conditioning has an effect on myocardial contractile function following an acute myocardial infarction []. Again, mitochondria play a major role as ischemic conditioning improves respective preserves mitochondrial respiration, ATP production and calcium handling. However, while effects on mitochondria have been shown, the long term effects of ischemic conditioning need further evaluation. The authors review in their manuscript the current knowledge and elucidate where further investigations are needed.