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Contemporary Review in Critical Care Medicine:Mitochondria and Critical Illness

Gerald S Supinski, Elizabeth A Schroder, Leigh Ann Callahan
Chest 2019 September 5
31494084
Classically, mitochondria have largely been thought to influence the development of illness by modulating cell metabolism and determining the rate of production of high energy phosphate compounds (e.g. ATP). It is now recognized that this is a simplistic view and that mitochondria play key roles in many other processes, including cell signaling, regulating gene expression, modulating cellular calcium levels and influencing the activation of cell death pathways (e.g. caspase activation). Moreover, these multiple mitochondrial functional characteristics are now known to influence the evolution of cellular and organ function in many disease states, including sepsis, ICU acquired skeletal muscle dysfunction, acute lung injury, acute renal failure, and critical illness related immune function dysregulation. In addition, diseased mitochondria generate toxic compounds, most notably released mitochondrial DNA, which can act as Danger Associated Molecular Patterns (DAMPS) to induce systemic toxicity and damage multiple organs throughout the body. This paper will review these evolving concepts relating mitochondrial function and acute illness and will organize this discussion into four sections: (I) basics of mitochondrial physiology, (II) cellular mechanisms of mitochondrial pathophysiology, (III) critical care disease processes whose initiation and evolution are shaped by mitochondrial pathophysiology, and (IV) emerging treatments for mitochondrial dysfunction in critical illness.

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