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BioMed Research International
Volume 2017, Article ID 7897325, 12 pages
Review Article

Skeletal Muscle and Lymphocyte Mitochondrial Dysfunctions in Septic Shock Trigger ICU-Acquired Weakness and Sepsis-Induced Immunoparalysis

1Hôpitaux Universitaires de Strasbourg, Hôpital de Hautepierre, Service de Réanimation Médicale, avenue Molière, 67098 Strasbourg Cedex, France
2Université de Strasbourg, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Faculté de Médecine, Institut de Physiologie, Equipe d’Accueil 3072 “Mitochondrie, Stress Oxydant et Protection Musculaire”, 11 rue Human, 67000 Strasbourg, France
3Hôpitaux Universitaires de Strasbourg, Hôpital de Hautepierre, Service d’Anesthésie-Réanimation Chirurgicale, avenue Molière, 67098 Strasbourg Cedex, France
4Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR7104, INSERM U964, Université de Strasbourg, Illkirch, France
5Hôpitaux Universitaires de Strasbourg, Nouvel Hôpital Civil, Service de Physiologie et d’Explorations Fonctionnelles, 1 Place de l’Hôpital, 67091 Strasbourg Cedex, France

Correspondence should be addressed to Julien Pottecher; rf.gruobsarts-urhc@rehcettop.neiluj

Received 1 February 2017; Revised 16 March 2017; Accepted 23 April 2017; Published 15 May 2017

Academic Editor: Thomas Griffith

Copyright © 2017 Quentin Maestraggi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Fundamental events driving the pathological processes of septic shock-induced multiorgan failure (MOF) at the cellular and subcellular levels remain debated. Emerging data implicate mitochondrial dysfunction as a critical factor in the pathogenesis of sepsis-associated MOF. If macrocirculatory and microcirculatory dysfunctions undoubtedly participate in organ dysfunction at the early stage of septic shock, an intrinsic bioenergetic failure, sometimes called “cytopathic hypoxia,” perpetuates cellular dysfunction. Short-term failure of vital organs immediately threatens patient survival but long-term recovery is also severely hindered by persistent dysfunction of organs traditionally described as nonvital, such as skeletal muscle and peripheral blood mononuclear cells (PBMCs). In this review, we will stress how and why a persistent mitochondrial dysfunction in skeletal muscles and PBMC could impair survival in patients who overcome the first acute phase of their septic episode. First, muscle wasting protracts weaning from mechanical ventilation, increases the risk of mechanical ventilator-associated pneumonia, and creates a state of ICU-acquired muscle weakness, compelling the patient to bed. Second, failure of the immune system (“immunoparalysis”) translates into its inability to clear infectious foci and predisposes the patient to recurrent nosocomial infections. We will finally emphasize how mitochondrial-targeted therapies could represent a realistic strategy to promote long-term recovery after sepsis.