Send to

Choose Destination
Shock. 2016 Mar;45(3):271-81. doi: 10.1097/SHK.0000000000000463.


Author information

*Bloomsbury Institute of Intensive Care Medicine, University Hospital London, UK †Department of Pediatrics and Molecular Medicine, Hofstra-North Shore-Long Island Jewish School of Medicine, New Hyde Park, New York ‡Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania §Departments of Pediatrics-Neonatology, Cell and Molecular Biology and Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois ||Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania ¶Center for Critical Care Nephrology, University of Pittsburgh, Pittsburgh, Pennsylvania #Academia Colombiana de Medicina Critica (ACOMEC) **Division of Critical Care Medicine, Clínica Palermo, Bogotá, Colombia ††University College Dublin, Dublin, Ireland.


Mitochondria are an essential part of the cellular infrastructure, being the primary site for high-energy adenosine triphosphate production through oxidative phosphorylation. Clearly, in severe systemic inflammatory states, like sepsis, cellular metabolism is usually altered, and end organ dysfunction is not only common, but also predictive of long-term morbidity and mortality. Clearly, interest is mitochondrial function both as a target for intracellular injury and response to extrinsic stress have been a major focus of basic science and clinical research into the pathophysiology of acute illness. However, mitochondria have multiple metabolic and signaling functions that may be central in both the expression of sepsis and its ultimate outcome. In this review, the authors address five primary questions centered on the role of mitochondria in sepsis. This review should be used both as a summary source in placing mitochondrial physiology within the context of acute illness and as a focal point for addressing new research into diagnostic and treatment opportunities these insights provide.

[Available on 2017-03-01]
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wolters Kluwer Icon for PubMed Central
Loading ...
Support Center