This article is part of a series on Sepsis, edited by Bruno Levy.

Review

Bench-to-bedside review: Potential strategies to protect or reverse mitochondrial dysfunction in sepsis-induced organ failure

Alessandro Protti^1,2 and Mervyn Singer¹

¹Bloomsbury Institute of Intensive Care Medicine, Wolfson Institute for Biomedical Research and Department of Medicine, University College London, London, UK

²Istituto di Anestesia e Rianimazione, Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena – IRCCS, Milan, Italy

author email corresponding author email

Critical Care 2006, 10:228doi:10.1186/cc5014

Published:	1 September 2006

Abstract

The pathogenesis of sepsis-induced multiple organ failure may crucially depend on the development of mitochondrial dysfunction and consequent cellular energetic failure. According to this hypothesis, interventions aimed at preventing or reversing mitochondrial damage may have major clinical relevance, although the timing of such interventions will be critical to both ensuring benefit and avoiding harm. Early correction of tissue hypoxia, strict control of glycaemia, and modulation of oxidative and nitrosative stress may afford protection during the initial, acute systemic inflammatory response. The regulated induction of a hypometabolic state resembling hibernation may protect the cells from dying once energy failure has developed, allowing the possibility of functional recovery. Repair of damaged organelles through stimulation of mitochondrial biogenesis and reactivation of cellular metabolism may accelerate resolution of the multiple organ failure syndrome.